








































































































































































































































































































































































COPYRIGHT DEPOSIT. 


























































































Clinical Medicine 
for Nurses 


/ 



PAUL H. RINGER, A.B., M.D. 

v\ 

Chief of Medical Service of the Asheville Mission Hospital, 
Asheville, N. C.; on staff of Biltmore Hospital, 
Biltmore, N, C. 


ILLUSTRATED 


SECOND REVISED EDITION 



PHILADELPHIA 

F. A. DAVIS COMPANY, Publishers 
1924 






TO‘ 


COPYRIGHT, 1918 
COPYRIGHT, 1924 

BY 

F. A. DAVIS COMPANY 


Copyright, Great Britain. All Rights Reserved 



©Cl AS07626 

PRINTED IN U. S. A. 
PRESS OF 

F. A. DAVIS COMPANY 
PHILADELPHIA, PA. 


NOV - 3 *24 




TO THE NURSES OF THE 
ASHEVILLE MISSION HOSPITAL, ASHEVILLE, N. C., 

WHOSE NEED HAS BEEN THE MAIN 
STIMULUS TO THE WRITING 
OF THIS VOLUME. 






PS 5 

— 

























































































PREFACE TO SECOND EDITION 


The general scheme of this book has in no way 
been altered. A goodly number of minor changes 
have been made, however, and some sections wholly 
or partially rewritten, notably those on the treatment 
of Heart-failure, Influenza, and Diabetes Mellitus. A 
short section on Auricular Fibrillation has been in¬ 
troduced and Eggleston’s method of full Digitaliza¬ 
tion of the heart has been briefly explained. The 
classification of nephritis has been changed, a slightly 
simplified modification of Christian’s excellent scheme 
having been adopted. Some errors have been elim¬ 
inated. It is hoped that no new ones have crept in. 

Paul H. Ringer. 

16 Haywood St., 

Asheville, N. C. 


(v) 




PREFACE TO FIRST EDITION 


The following chapters represent the substance of 
lectures on medical diseases that I have delivered for 
several years at the Asheville Mission Hospital. 

I have been impelled to write them out, as in no text¬ 
book for nurses that I have seen did I feel that the 
subjects were taken up in sufficient detail, while in all 
textbooks on medicine there were far too many minutiae 
for the pupil nurse to attempt to master. 

The object of these lectures is to place in concrete 
form a fairly detailed description of the points in the 
various diseases that nurses will be expected to ob¬ 
serve and interpret, and also to form a basis upon 
which class-room lessons can be assigned and quizzes 
held, the teacher amplifying as he sees fit. 

It will be noted that the bacteriology and pathology 
of diseases, save in a very few instances, have been 
but sketchily traced. The main points dwelt upon 
have been symptoms and their meaning, complications 
and their detection, as far as the nurse is concerned. 
Physical signs have been wholly set aside. I do not 
feel that any nurse’s mind should be burdened with 
their description and significance. 

Treatment has been dealt with in a general manner, 
it being ever borne in mind that each physician has his 
own preference for the treatment of almost every dis¬ 
ease, and that such preference should not be infringed 
upon in a textbook intended solely for teaching purposes 



PREFACE. 


viii 

by physicians with varied ideas. I do not believe that 
any of the principles set forth will seriously offend. 

The subject matter of the lectures has no claim 
whatsoever to originality. I have freely consulted 
the best authorities at my command, abstracting here 
and there in order to produce a concrete whole. The 
only claim that these lectures have for individuality 
lies in their being, as far as I know, the first collec¬ 
tion of lectures covering a considerable number of 
medical diseases delivered for and to nurses. 

Paul H. Ringer. 

Asheville, N. C. 


CONTENTS 


CHAPTER PAGE 

I. Fever . 1 

II. Food and Nutrition . 4 

III. The Circulation . 13 

IV. Rheumatic Fever. 21 

V. Pericarditis . 30 

VI. Endocarditis (Acute Simple and Malignant) .. 36 

VII. Endocarditis (Chronic) . 42 

VIII. Myocarditis and Aneurysm of the Aorta. 59 

IX. Blood-pressure . 66 

X. The Urine. 72 

XI. Uremia . 82 

XII. Nephritis (Bright’s Disease) . 87 

XIII. Chronic Nephritis With Edema . 97 

XIV. Chronic Nephritis Without Edema and Arter¬ 

iosclerosis . 101 

XV. Tests of Kidney Efficiency (Renal Function 

Tests) . 109 

XVI. Cerebral Hemorrhage (Apoplexy) and Cerebral 

Thrombosis . US 

XVII. Pleurisy (Dry and with Effusion) . 119 

XVIII. Lobar Pneumonia . 126 

XIX. Bronchopneumonia . 142 

XX. Influenza . 147 

XXI. Typhoid Fever . 155 

XXII. Tuberculosis . 188 

XXIII. Scarlet Fever.'. 221 

XXIV. Measles . 229 

(ix) 


























X 


CONTENTS. 


CHAPTER PA GE 

XXV. Diphtheria . 233 

XXVI. Anterior Poliomyelitis (Infantile Paralysis) .. 241 

XXVII. Epidemic Cerebrospinal Meningitis . 246 

XXVIII. Syphilis . 251 

XXIX. Locomotor Ataxia . 257 

XXX. Diabetes Mellitus . 260 

XXXI. The blood. 272 

XXXII. Pernicious Anemia and Leukemia . 278 

XXXIII. Exophthalmic Goitre (Graves’s Disease) . 282 

XXXIV. Immunity . 286 

Glossary . 291 

Index . 301 













CHAPTER I. 

FEVER.* 

Probably the most common single symptom of acute 
disease is fever. It would be unwise and undesirable to 
go at any length into the origin of fever, for it is veiled 
in much mystery and in many theoretical considerations; 
suffice it to say that it occurs in various degrees of in¬ 
tensity in a host of maladies, that it is one of the best 
signs we have of disturbance in the human body, and that 
it is the one symptom above all others that by its presence 
speaks for the existence of some pathological condi¬ 
tion, though giving usually no clue to the location of the 
trouble. 

Fever, itself, while called a “symptom,” is really a 
“symptom-complex,” being a very complete clinical en¬ 
tity, quite irrespective of the underlying cause. The ordi¬ 
nary symptoms of fever of moderate severity ( e.g ., 
103°) are: 

Hot, dry skin. 

Flushed face. 

Bright, anxious eyes. 

Thirst. 

Full, rapid and bounding pulse. 

Rapid and rather shallow respiration. 

Headache. 

Anorexia. 

General aching in body and limbs. 


* Throughout this book the Fahrenheit scale is used, unless 
otherwise specified. 


1 


(i) 



2 


CLINICAL MEDICINE FOR NURSES. 


Nausea and vomiting (not very frequently). 

Constipation or diarrhea (usually the former). 

Scant, high-colored urine. 

Of course, at times some of these symptoms will be 
more intense, and at times others, but in the main all of 
them will be present to some extent. When the tempera¬ 
ture rises to 105° or over, or even below this limit in 
susceptible individuals, delirium may occur. This may 
be accompanied by convulsions, especially in children. 
Should the patient be extremely toxic, coma may set in 
—always a very serious sign. 

Fever may be: 

1. Continuous, e.g., scarlet fever. 

2. Remittent, a fever that shows rises and falls, but 

that never wholly leaves the patient, e.g., ty¬ 
phoid fever, septic fevers. 

3. Intermittent, a fever that seizes! the patient, and 

then wholly disappears, only to return again, 
e.g., the fever in tertian and quartan malaria. 

Fever may begin: 

1. Suddenly, e.g., lobar pneumonia. 

2. Gradually, e.g., typhoid fever. 

Fever may end: 

1. By crisis, i.e., suddenly; e.g., lobar pneumonia. 

2. By lysis, i.e., gradually; e.g., typhoid fever, 

measles. 

Fever is divided into the following classes by Wunder¬ 
lich : 

1. Subfebrile, 99.5° to 100.4°. 

2. Slightly febrile, 100.4° to 101.3°. 

3. Moderately febrile, 101.3° to 103.1°. 

4. Decidedly febrile, 103.1° to 104°. 


FEVER. 


3 


5. Highly febrile, above 103.1° in the morning and 

above 104.9° in the evening. 

6. Hyperpyretic, above 106°. 

There is usually a certain ratio between the height of 
the temperature and the pulse-rate. Thus, generally 


speaking 

A temperature of 98.4 corresponds to a pulse-rate of 70 


“ 

a 

“ 100. 

a 

u u 

a 

“ 80- 90 

it 

it 

“ 102. 

“ 

“ “ 

a 

“ 100-110 

u 

“ 

“ 104. 

u 

it u 

a 

“ 120-130 


These rules are capable of the utmost variation. 


CHAPTER II. 
FOOD AND NUTRITION. 


All food may be regarded as fuel, and the body as 
the furnace in which it is consumed. The object of food 
is to supply nutriment to the body, and this nutriment 
is used in the production of heat and energy. When 
taken into the body, food undergoes the following 
processes: 

1. Digestion. 

2. Absorption. 

3. Oxidation. 

4. Excretion. 


6 per cent, of body weight. 


There are five main classes of foodstuffs: 

1. Proteins. 

2. Fats. 

3. Carbohydrates. 

4. Mineral salts of 

(w) Calcium 

(*■) Sodium 

(y) Potassium 

(z) Magnesium 

5. Water—60 per cent, of food, and serving, among 

other things, to keep the body at a proper con¬ 
sistency. 

1. Proteins. These include all foodstuffs containing 
nitrogen (N), and are absolutely indispensable to the 
maintenance of life. An animal fed on a protein-free 
diet, no matter how generous or how abundant it may be, 
eventually starves to death. 

(4) 



FOOD AND NUTRITION. 


5 


Proteins are divided into several sub-classes, but three 
of which will be mentioned: 

I. Albuminoids. 

(a) White of egg. 

( b ) Curd of milk. 

( c ) Lean of meat. 

( d ) Gluten of wheat. 

II. Gelatinoids. 

Gelatin the best example. 

III. Extractives. 

Contain nitrogen, but differ from the two 
preceding in that they merely add zest 
to the food, but have practically no 
nutritive value. 

2. Fats. Fats, roughly speaking, make up about 15 
per cent, of the average individual, and are generally 
taken into the body in the form of: 

Butter. 

Cream. 

Oils. 

The amount of fat varies very greatly in different in¬ 
dividuals. 

3. Carbohydrates. These substances are formed of 
carbon (C), hydrogen (H) and oxygen (O), the last two 
always appearing in the proportion to form water—H 2 0. 
Thus, starch has the chemical formula C 6 H 10 O 5 . It will 
be noted that the atoms of H are just twice as numerous 
as those of O; thus we have the proportion H 2 0. Bread, 
rice, and potato are examples of carbohydrate foods. 

Object of Various Foodstuffs. 

1. Proteins. These are to build up tissue, and to a cer¬ 
tain extent to be converted into other foodstuffs, such as 


6 


CLINICAL MEDICINE FOR NURSES. 


fat and carbohydrate. They also serve as fuel to yield 
heat and muscular power. 

2. Fats. These form an abundant source of heat and 
energy. They are also useful in serving as a buffer to 
the body at various points where much friction occurs, 
and in addition form the main reserve and storehouse 
upon which the body can make demands in times of 
necessity. Thus, when food is withheld, the body needs 
are primarily supplied by the overplus of 1 fat. The 
emaciation consequent upon long illness is chiefly due to 
the oxidation and using up of the reserve store of fat. 

3. Carbohydrates. In addition to their intrinsic food 
value, these substances may be transformed into fats, and 
used as such, or else they may be used as fuel to supply 
the immediate body needs. 

As mentioned above, protein is the substance without 
which life cannot be sustained. Protein can, to a certain 
extent, be transformed into fat and carbohydrate, and, 
as seen above, carbohydrate can be transformed into fat; 
but neither fat nor carbohydrate can in any way be trans¬ 
formed into protein, for neither of them contains the 
all-important element, nitrogen. Hence, a protein-free 
diet amounts in the long run to starvation, and, if per¬ 
sisted in for a sufficient length of time, proves fatal. 

From the foregoing it must not be imagined that a 
fat-free or a carbohydrate-free diet would in any way 
prove nourishing, beneficial or healthful. All three 
classes of foodstuffs are of paramount importance to the 
human body, and must be taken in certain well-defined 
general proportions; but stress must be laid on the fact 
that protein is an absolute necessity. 

The energy and heat of the body are derived from 
the combustion of its foodstuffs. As energy can be con- 


FOOD AND NUTRITION. 


7 


verted into heat, the value of foodstuffs can be expressed 
in heat units. The heat unit is called calorie. A calorie 
is that amount of heat needed to raise a kilogram of 
water to one degree Centigrade. 

The amount of heat given off from the human body 
has been measured with accuracy. In a condition of 
rest, a man gives off heat in twenty-four hours equiva¬ 
lent to about 33 calories per kilogram (2.2 pounds) of 
body weight. Thus, a man weighing 70 kilos (154 
pounds) gives off about 2310 calories (70 X 33). This 
amount must be supplied by foodstuffs in order to main¬ 
tain a satisfactory state of nutrition. It has been calcu¬ 
lated that these 2310 calories must contain about 500 
Gm. of carbohydrate, 50 to 100 Gm. of fat, and 120 Gm. 
of protein. 

1 Gm. of protein produces 4 calories. 

1 Gm. of fat produces 9 calories. 

1 Gm. of carbohydrate produces 4 calories. 

Rubner gives the following standard dietary for a man 
of 70 kilos (154 lbs.): 


Protein Gm. 

Fat Gm. 

Carbohydrate Gm, 
Calories . 


Light 

Medium 

Heavy 

work 

work 

work 

.. 123 

127 

165 

.. 46 

52 

70 

.. 377 

509 

565 

.. 2445 

2868 

3362 


Thus it will be seen that the average man doing med¬ 
ium work requires about 127 Gm. of protein daily. Not 
much more than 150 Gm. can be given without the ap¬ 
pearance of symptoms of overfeeding—gastric or intes¬ 
tinal derangements. In feeding any individual, the point 






8 


CLINICAL MEDICINE FOR NURSES. 


to be borne in mind is not so much the maximum or 
minimum number of calories which the patient will toler¬ 
ate, or upon which he can exist, as that amount upon 
which the patient will thrive best. 

The following table gives the daily needs in calories 
of an adult weighing 65 kilos (162.5 lbs.) : 


1. During rest in bed 1800 cal., or 28 cal. per kilo of body wt. 


2. In repose 

3. Light work 

4. Moderate work 

5. Hard work 


2100 “ “ 32 “ 

2300 “ “ 33 “ 

2600 “ “ 40 “ 

3100 “ “ 48 “ 


t u a a a 

% a a a a 

i u a a u 

» f ii m a u a 


Infants require more calories per kilo of body weight 
than do adults. This can readily be accounted for when 
we consider the tremendous growth and consequent tis¬ 
sue changes taking place in the infant. 

For 1st 3 mos. an infant requires 100 cal. per kilo of body wt. 

“ 2d 3 “ “ “ “ 90-100 “ “ “ “ 

“ 2d 6 “ “ “ “ 80 “ “ “ “ “ 


Average cow’s milk contains 320 calories per pint (640 
calories per quart). Eggs contain about 720 calories per 
pound, the whites alone yielding 250 calories per pound, 
and the yolks 1705 calories per pound. The white is pure 
protein, while the yolk contains numerous substances, 
chief of which are: 15 per cent, protein, 20 per cent, 
fat, besides lecithin, nuclein, salts of iron, calcium, 
potassium, and magnesium. 

Meats are best prepared by broiling or roasting. Bouil¬ 
lons and beef extracts consist mainly of extractives from 
the meat, and, contrary to an idea, almost universally 
prevalent among the laity, have practically no food value. 
The following table gives the caloric value per pound 
of the principal meats: 


FOOD AND NUTRITION. 


9 


Calories 


Beef (steak) . 975 

Veal . 745 

Mutton . 890 

Lamb . 1075 

Pork chops . 1245 

Chicken (broilers) . 305 

Turkey . 1060 


Vegetables contain a large percentage of starch and 
sugar, and a somewhat lesser percentage of protein. 

The number of calories needed daily by a man in health 
has been dwelt upon in some detail. When an individual 
is suffering with fever from any cause, from 20 to 30 
per cent, more heat is given off than in health. This 
must be made good by an increased caloric intake, or the 
patient will suffer. Especially is this true in long fevers, 
such as those caused by typhoid, tuberculosis, and rheu¬ 
matic fever. In the shorter fevers, such as lobar pneu¬ 
monia, the maintenance of the bodily strength by means 
of increased caloric feeding is not so important. If 25 
per cent, be added to the normal amount required by the 
average man (2300 calories in 24 hours), we see that 
during fever from 2800 to 2900 calories in 24 hours will 
be needed. 

Foods whose caloric value is not very great can have 
that value raised by the addition of substances whose 
caloric value is very high, such as milk sugar (caloric 
value per ounce, 117) and cream (caloric value per 
ounce, 54). Qualitative changes can be made in foods 
which will counteract the enormous quantity that would 
have to be ingested to supply the caloric needs were the 
food, as such, given. For instance, if in a case of typhoid 
reliance were placed solely on a milk diet, and the stock 
order, “a glass of milk every two hours” carried into 









10 


CLINICAL MEDICINE FOR NURSES. 


effect, the patient would be wretchedly under-nourished. 
A glass of milk contains from 6 to 8 ounces. One quart 
of milk produces 640 calories. Ten feedings will be 
about all the patient will get in 24 hours. He will, there¬ 
fore, be given from 60 to 80 ounces of milk—practically 
two quarts, 1280 calories—two-thirds of what he should 
really have. To meet the needs of the patient, five quarts 
of milk daily would be required. 

Latterly, the so-called-“high-calorie diet” has been used 
with marked success in the treatment of typhoid fever, 
further reference to which will be made in the chapter 
on that disease. 

Administration of Food to the Sick. 

Details—one might almost say trivialities—are of the 
greatest importance, and are too often not sufficiently 
heeded by the nurse. Florence Nightingale wrote: “To 
watch for the opinions which the patient’s stomach gives 
rather than to read ‘analyses of foods’ is the business of 
all those who have to settle what the patient is to eat— 
perhaps the most important thing to be provided for him 
after the air he breathes. * * * An almost universal 

error among nurses is the bulk of the food, and especially 
of the drinks, they offer to their patients. It requires very 
nice observation and care (and meets with hardly any) 
to determine what will not be too thick or too strong for 
the patient to take, while giving him no more than he is 
able to swallow.” 

The following are some important points to be noted 
in the feeding of the sick: 

1. Punctuality. To the invalid meal-time is an import¬ 
ant event. He looks forward to it with interest and with 


FOOD AND NUTRITION. 


11 


curiosity. He eyes the clock a hundred times until the 
arrival of the appointed hour. When that hour comes, 
the meal also should come. Waiting until the stated time 
tends to sharpen the patient’s appetite; waiting beyond 
that time disappoints, irritates, and tends markedly to 
blunt the desire for food. 

2. Do not ask the patient with a poor appetite what he 
wants to eat. He does not want anything, and if foods 
are named to him and his suggestions invited, his repug¬ 
nance becomes increased. His appetite can best be stim¬ 
ulated by exciting his surprise and curiosity. 

3. Untasted food, dishes after use, half-emptied cups 
and glasses, should never be left in the sick-room. They 
are unsanitary, and often tend to nauseate the sensitive 
patient. There is nothing more frequently seen in the 
sick-room, and there are few things more disgusting, 
than an empty, unwashed glass that has contained milk. 

4. Wipe dishes dry on the outside, and take special 
care that the contents of cups are not spilled into the 
saucers. 

5. Mutton or chicken broth should be skimmed sev- 
eral times before serving. Blotting paper or a piece of 
thread can be passed over the surface to remove the last 
traces of oily substance. 

6. When the dietary is limited, or the appetite is poor, 
it is often well to serve the meal in “courses.” Time 
after time the writer has had patients complain that they 
lost all desire for food at once after the appearance of a 
large tray loaded down with all sorts of eatables, from 
soup to dessert. Many of these same patients would 
have eaten well and with enjoyment had the same food 
been daintily served, one course at a time. 


12 


CLINICAL MEDICINE FOR NURSES. 


7. Do not offer food to the patient immediately after a 
bowel or bladder evacuation. If the patient has just used 
the bed-pan or urinal, the nurse should make it very ap¬ 
parent that she has thoroughly cleansed her hands be¬ 
fore busying herself with food. 


CHAPTER III. 


THE CIRCULATION—GENERAL CONSIDERATIONS. 

The vascular system in and through which the blood 
circulates consists of a central pump (the heart) and a 
system of tubes of three distinct types: 

1. Arteries. Vessels carrying blood away from the 
heart, becoming progressively smaller as their distance 
from the heart increases, having walls relatively thick, 
rich in elastic fibres, by the recoil of which the blood 
stream generated by the force of the heart-beat is kept 
in motion, and in which the blood is kept at a relatively 
high degree of pressure. 

2. Capillaries. Microscopic vessels everywhere per¬ 
meating the tissues, lined by a single layer of cells, 
through the walls of which the food and oxygen brought 
by the blood are taken up by the tissues, and the waste 
products to be gotten rid of by the organs of elimination 
are given off. 

3. Veins. Relatively large vessels, in comparison with 
the arteries, becoming progressively larger as.they ap¬ 
proach the heart, bearing stale and deoxygenated blood 
toward the heart, having thin walls, poor in elastic fibres 
and easily collapsible, containing the blood under very 
low pressure, and possessing at frequent intervals small 
valves to prevent any appreciable back-flow of blood. 

The circulation—regular, incessant, and rhythmic—of 
the blood in this closed system of tubes was first dis¬ 
covered and demonstrated by William Harvey in 1616. 
In order to better understand the meaning and causation 

(13) 


14 


CLINICAL MEDICINE FOR NURSES. 


of symptoms in many diseases to be dealt with later, a 
glance into the realm of the physiology and mechanics of 
the circulation is desirable. 

Course of the Circulation. 

Left ventricle. 

Aorta. 



Fig. 1.—General diagram of the circulation: the arrows 
indicate the course of the blood; PA, pulmonary artery; PC, 
pulmonary capillaries; PV, pulmonary veins; LA, left auri¬ 
cle; LV, left ventricle; A, systemic arteries; C, systemic cap¬ 
illaries; V, systemic veins; RA, right auricle; RV, right ven- - 
tricle. (From “Howell’s Physiology,” W. B. Saunders Co.) 

Systemic arteries. 

Systemic capillaries. 

Systemic veins (some blood deflected through portal 
system; vide infra). 

Inferior and superior venae cavae. 






THE CIRCULATION. 


15 


Right auricle. 

Right ventricle. 

Pulmonary artery (containing venous blood), named 
“artery” because it carries blood away from the 
heart. 

Pulmonary capillaries (lungs). 

Pulmonary veins (4) (containing arterial blood), 
named “veins” because they bring blood toward 
the heart. 



Fig. 2.—Diagram of the portal system: the arrows indi¬ 
cate the course of the blood; A, arterial system; V, venous 
system; C, capillaries of the spleen, pancreas, and alimentary 
canal; PV, portal vein; C", capillaries of the liver; C', the 
rest of the systemic capillaries. The hepatic artery is not 
represented. (From “Howell’s Physiology,” W. B. Saunders 
Co.) 

Left auricle. 

Left ventricle. 

Subdivisions of the Circulation. 

1. Greater or systemic. Includes all arteries, capil¬ 
laries and veins throughout the body, except those going 
to and from the lungs and those vessels uniting to form 
the portal system ( q.v .). 








16 


CLINICAL MEDICINE FOR NURSES. 


2. Lesser or pulmonary. Includes the pulmonary ar¬ 
tery, the pulmonary capillaries and the four pulmonary 
veins—in other words, all those vessels in which the 
blood is contained from the time it leaves the right ven¬ 
tricle until it enters the left auricle. 

3. Portal or splanchnic. Includes those veins (and 
veins only) which drain the alimentary tract, and whose 
blood, consequently, is more filled with waste products 
than is that from other portions of the body. These 
veins—the so-called “radicals”—of the portal system join 
to form the portal vein which, in company with the 
hepatic artery and the common bile duct, enters the liver 
embedded in the capsule of Glisson, and iii the liver 
breaks up into branches, and delivers its blood to that 
organ to be further purified before leaving through the 
hepatic vein to proceed onward toward the heart. 

The physiology of the circulation, especially that of the 
lesser or pulmonary circulation, is so intimately blended 
with the fundamentals of the physiology of respiration 
that a few lines on that subject will not be amiss. 

Respiration and the lungs provide for an exchange of 
gases between the blood on the one hand and the external 
air on the other. The blood coming to the pulmonary 
capillaries from the right side of the heart via the pul¬ 
monary artery, is blood that has made its rounds of the 
circulation, has given up to the tissues the oxygen that 
it had acquired at its previous passage through the lungs, 
and has taken unto itself instead waste products ab¬ 
sorbed from the tissues during its passage through them. 
It must now yield up its waste products, and take unto 
itself a new supply of oxygen. This can be done in the 
pulmonary capillaries. These microscopical vessels have 
walls of extreme thinness, and through the single layer 


THE CIRCULATION. 


17 


of endothelial cells forming these walls the interchange of 
gases takes place during the few seconds that any given 
red blood corpuscle is flowing through the lungs. 

The blood corpuscle gives off carbon dioxide (C0 2 ), 
and in exchange receives a full charge of oxygen from 
the air inspired during its sojourn in the lungs. Re¬ 
freshed and ready for its duty, the corpuscle is then car¬ 
ried by the pulmonary veins to the left side of the heart, 
whence it is started on its trip over the body to give up 
in turn to the needy tissues the oxygen without which 
they cannot live. 

The air in the alveoli or terminal chambers of the lungs 
is kept fresh and ever changing by the respiratory move¬ 
ments, pure air, rich in oxygen being inspired, and stale 
air being expired. 

The Heart. The heart, or central pump, power-house 
and motive force of the entire circulatory system, de¬ 
mands notice. It is composed of muscle, striated, but 
involuntary—that is to say, possessing the striae common 
to voluntary muscles, but being quite beyond the power 
of the will, though most susceptible to the emotions. 

The heart contains four cavities or chambers. The 
two upper and smaller ones are the auricles, right and 
left, respectively. The two lower and larger ones are 
the ventricles, also right and left, respectively. The right 
auricle opens directly into the right ventricle, and the 
left auricle into the left ventricle. The superior and in¬ 
ferior venae cavae open into the right auricle. The pul¬ 
monary artery opens out from the right ventricle. The 
four pulmonary veins, two from each lung, open into the 
left auricle. The left auricle empties directly into the left 
ventricle; and the aorta, the main arterial trunk of the 
body, emerges from the upper part of that chamber. 

2 


18 


CLINICAL MEDICINE FOR NURSES. 


The Cardiac Cycle. From the beginning of one beat 
of the heart to the beginning of the next succeeding beat 
constitutes a “cardiac cycle.” The cardiac cycle is 
divided into two main parts: 

1. Systole —the work portion of the cycle—that por¬ 
tion during which the auricles and ventricles contract and 
drive the blood onward. 

2. Diastole —the rest portion of the cycle—that por¬ 
tion during which the cavities of the heart are being filled 
with blood which will be forced onward at the next 
systole. 

The contractions of auricles and ventricles do not take 
place at exactly the same time, the auricles contracting 
immediately before the ventricles. 

The ordinary complete cardiac cycle with the heart 
beating 72 times to the minute, lasts eight-tenths of a 
second. Of this: 

( 4 :) Auricular systole lasts 0.1 second. 

(y) Ventricular systole lasts 0.3 second. 

(£) Diastole lasts 0.4 second. 

Thus it is seen that 50 per cent, of the time is spent by 
the heart in resting. When we consider that from birth 
to death the heart never has what in the ordinary sense 
we construe as “rest,” the importance of this recupera¬ 
tive portion of the cardiac cycle is at once apparent. 

The vagus nerve exercises an important inhibitory or 
slowing effect upon the heart. It acts as a brake, and 
prevents the heart from running away with itself. Thus, 
it is another potent factor established by Nature for 
ensuring the heart’s obtaining enough rest. 

The Cardiac Valves. With this multiplicity of car¬ 
diac chambers and of vessels entering and leaving these 
chambers, there exists a most simple and unique means 


THE CIRCULATION. 


19 


of preventing the back-flow of blood, and of maintaining 
the mechanics of the circulation. This unique means con¬ 
sists in the valves of the heart. The valves of the heart 
are four in number: 

1. Mitral or bicuspid valve, situated between the left 
auricle and the left ventricle, opened automatically by the 
blood current during ventricular diastole, and similarly 
closed during ventricular systole, thus preventing regur¬ 
gitation of blood into the left auricle, and causing all the 
blood in the ventricular cavity to be discharged through 
the aorta and thus to reach the body generally. 

2 . Tricuspid valve, situated between the right auricle 
and the right ventricle, opened automatically by the blood 
current during ventricular diastole, and similarly closed 
during ventricular systole, thus preventing regurgitation 
of blood into the right auricle, and causing all the blood 
in the ventricular cavity to be discharged through the 
pulmonary artery, and thus to reach the lungs. 

It will thus be seen that the mitral and tricuspid valves 
open and close at the same time and act similarly, the 
former on the left and the latter on the right side of the 
heart. This also applies to the two sets of valves next to 
be considered. 

3. Aortic semilunar valves, situated at the emergence 
of the aorta from the left ventricle, automatically closed 
by the reflux of blood after ventricular systole, and re¬ 
maining closed during ventricular diastole, thus prevent¬ 
ing regurgitation of blood into the ventricular cavity, 
which is being filled anew from the left auricle; auto¬ 
matically opened by the blood current during ventricular 
systole to allow the passage of blood into the aorta. 

4. Pulmonary semilunar valves, situated at the emer¬ 
gence of the pulmonary artery from the right ventricle, 


20 


CLINICAL MEDICINE FOR NURSES. 


automatically closed by the reflux of blood in the pul¬ 
monary artery after ventricular systole, and remaining 
closed during ventricular diastole, thus preventing re¬ 
gurgitation of blood into the ventricular cavity, which 
is being filled anew from the right auricle; automatically 
opened by the blood current during ventricular systole to 
allow the passage of blood into the pulmonary artery. 

All the valves have three cusps or flaps save the mitral, 
which has but two. The flaps on the tricuspid and mit¬ 
ral valves are large and somewhat fan-shaped, of rather 
thick, fibrous structure, and covered with a glistening 
membrane, the endocardium, which is continuous with 
that lining the ventricular cavity. These cusps are con¬ 
nected with the ventricular walls by fine, cord-like proc¬ 
esses, the chordae tendince, and do not move freely in the 
blood current. 

The structure of the aortic and pulmonary semilunar 
valves is precisely similar. Both are composed of three 
flaps, each the shape of a half-moon, these three cusps 
meeting in the center of the lumen or calibre of the ves¬ 
sel when the valve is closed, and lying up against its 
wall when the valve is open. They are of much finer 
structure than are the auriculo-ventricular valves, are 
about the thickness of a piece of ordinary writing paper, 
translucent, and lined on their cardiac surfaces with a 
continuation of the endocardium that lines the ventric¬ 
ular cavity. 

These few physiological and anatomical facts will en¬ 
able us to better approach the clinical side of diseases 
and disturbances of the heart and circulatory system. 


CHAPTER IV. 


RHEUMATIC FEVER. 

Rheumatic fever has all the ear-marks of an acute 
infectious disease caused by a specific micro-organism. 
Hitherto the particular germ has resisted discovery, so 
the fundamental causative factor is not known. It is 
believed, however, to be a form of streptococcus. 
Rheumatic fever is intimately associated with the 
various diseases of the heart, to be taken up shortly. Dr. 
Olchin, a celebrated English clinician, has said that in 
adults rheumatic fever is a disease of the joints, with 
heart symptoms secondary, while in children rheumatic 
fever is a disease of the heart, with joint symptoms 
secondary. In any event, the connection between rheu¬ 
matic fever and pericarditis, endocarditis, and myocar¬ 
ditis is so close that it is the heart that must be watched 
first, last, and all the time. 

Etiology. Rheumatic fever attacks children and 
young adults in preference to those of riper years. 
Males are in the majority of those affected, and the dis¬ 
ease seems to have a predilection for those following cer¬ 
tain occupations, more especially drivers, servants, 
bakers, sailors, and laborers. It will be noted that these 
callings often necessitate prolonged exposure to the ele¬ 
ments, entail severe wettings, and in some cases, as in 
bakers, a sudden and marked change in temperature 
coupled with a damp atmosphere. These changes, as well 
as exposure, seem to be predisposing factors in the 
disease. . . 

(21) 



22 


CLINICAL MEDICINE FOR NURSES. 


Symptomatology. The onset of the disease is usually 
sudden. It may be preceded by a day or two of general 
malaise, accompanied by vague pains in the joints. Fre¬ 
quently it is ushered in by sore throat, and especially by 
tonsillitis. The patient may also have been a victim of 
chorea (St. Vitus’ Dance) which, with tonsillitis, seems 
to bear an important, though as yet unexplained, relation¬ 
ship to rheumatic fever. The temperature rises rapidly, 
and ranges between 102° and 104°. There are the accom¬ 
panying symptoms of fever, the tongue being moist, and 
covered with a white fur. There is loss of appetite, 
usually constipation, intense thirst, and scanty, highly 
colored urine. In the course of the disease, profuse acid 
sweats occur, which may have a sour odor. 

The Joints. The large joints are usually the ones in¬ 
volved, especially the knees, ankles, elbows, shoulders and 
wrists. Occasionally the articulations between the verte¬ 
brae may be the seat of inflammation. The affected 
joints are swollen, hot, red, tense, tender and exquisitely 
painful. At times their sensitiveness is so great that the 
tread of some one walking in the room, or the pressure 
of the bedclothes is unbearable. The swelling, pain, and 
tenderness last a variable time, from a few days to two 
weeks in any given joint; but it is characteristic of rheu¬ 
matic fever that while one joint is recovering another 
becomes involved, and thus the general picture of the 
disease may be prolonged several weeks. 

There is marked anemia and a leukocytosis, varying 
between 15,000 and 30,000. The disease may continue 
over many weeks, the fever being usually continuous, but 
not excessively high, and depending in its duration upon 
the joint involvement and upon the presence or absence 
of complications. The fall in the temperature is gradual, 


RHEUMATIC FEVER. 


23 


the symptoms slowly subsiding, leaving the patient much 
weakened and prostrated. 

The picture of a fully developed case of rheumatic 
fever, with its temperature and attendant symptoms, its 
drenching and exhausting sweats, its exquisitely painful 
joints, almost prohibiting all movement, and making each 
position assumed by the patient seem more agonizing 
than the preceding one, forms one of the most distress¬ 
ing sights in medicine. 

Complications. These are not great numerically, 
but are most important and severe. In fact, the terror 
of rheumatic fever lies not in the danger from the pri¬ 
mary disease itself, but in the complications that may, 
and unfortunately do, occur in a large percentage of 
cases. It is usually not the immediate, but the remote 
effects of acute rheumatic fever that are dreaded. 

Hyperpyrexia. A temperature from 105° to 108°; 
occurs most frequently in the second week, is an in¬ 
dication of grave toxemia, is often accompanied by de¬ 
lirium and stupor, and is most common in the first attack. 
It is always serious, and if prolonged and unrelieved 
may prove fatal. 

Cardiac Affections. These complications are among 
the most frequent and the most serious that are met with. 
According to Church, cardiac complications occurred in 
494 out of 889 cases—over 50 per cent. The heart con¬ 
ditions can be grouped under one of the three following 
heads: 

1. Endocarditis—valvular disease. 

2. Pericarditis. 

3. Myocarditis. 

The symptoms of these particular conditions will not 
be detailed here, as they are fully taken up under their 


24 


CLINICAL MEDICINE FOR NURSES. 


respective headings. Suffice it at this time to say that 
any change in the patient’s condition, not directly and 
unquestionably ascribable to the joints, should make the 
nurse consider the possibility of cardiac involvement and 
necessitates the utmost watchfulness. 

Pneumonia and Pleurisy. These complications occur 
in about 10 per cent, of the cases, and are characterized 
by their particular symptoms, the marked rise in tem¬ 
perature, shallow respiration, dyspnea and knife-like pain 
in one side being suggestive of pneumonia, while the 
pain without the marked onset of other symptoms is 
rather characteristic of pleurisy. 

Cerebral Complications: 

1. Delirium due to 

(.r) Hyperpyrexia. 

(y) Toxemia. 

Always serious, as denoting intense infection and 
lowered resistance. 

2 . Coma. More serious than the preceding, due to 

intense toxemia, and being an evidence of poor 
or exhausted defensive forces. 

3. Convulsions. Rare. 

Prognosis. The prognosis in rheumatic fever is al¬ 
ways grave, and is so, not because of the disease itself 
(for few die as a direct result of the rheumatic attack), 
but because of the frequency and severity of the com¬ 
plications. In fact, the outlook depends mainly upon the 
presence or absence of complicating factors. All cases 
with cardiac involvement must be looked upon as very 
seriously ill, and the outcome as very uncertain, as many 
weeks must elapse before it is possible to determine 


RHEUMATIC FEVER. 


25 


whether a cardiac inflammation will disappear com¬ 
pletely or else become chronic. In the first case, the out¬ 
look is good; in the second, though life may be prolonged 
many years, a permanently damaged organ exists, cure is 
out of the question, and the ultimate outlook is, therefore, 
bad. 

Treatment. The treatment of a patient suffering 
from an attack of rheumatic fever may be grouped under 
two general heads: 

1. Treatment of the general infection. 

2. Drug, or specific treatment of the infection. 

1 . (a) Rest. The patient with rheumatic fever should 
from the start, be confined absolutely to bed, the use 
of the bed-pan insisted upon, and no permission given 
for the patient to sit up in any way. There are three 
main reasons for insistence upon absolute rest: 

(„r) The body cells are the victims of an intoxi¬ 
cation. 

(y) Certain tissues in the body (the joints and pos¬ 
sibly the endocardium, pericardium, and myo¬ 
cardium) are undergoing alterations inci¬ 
dent to inflammation. 

(#) The likelihood of cardiac complications is re¬ 
duced by absolute rest. 

( b ) The Bed. If the patient perspires freely, the bed 
should be made with blankets instead of sheets, and the 
nurse should always bear in mind that, especially in a dis¬ 
ease of this nature, where pressure and movement cause 
such agonizing pain, the bed should be made with more 
regard to the comfort of the patient than to symmetry 
of appearance. It is not harmful to allow cold air in the 


26 


CLINICAL MEDICINE FOR NURSES. 


room, but care should be taken that at such times the 
patient is well covered. If the bedclothes cause pain, it 
may be necessary to make cradles out of barrel hoops 
or wire. 

The patient should wear a thin flannel nightgown, 
open down the front, and slit up the sleeves, so as to ad¬ 
mit of easy inspection of joints and heart. Flannel is far 
more welcome than cotton., because it does not become 
cold and clammy after sweats. 

(c) Diet. This should be fairly liberal, small amounts 
frequently given being more desirable than larger 
amounts at longer intervals, and reliance should be placed 
mainly in the following articles: milk, soups, cereals, cus¬ 
tard, bread, rice. Acids should be wholly avoided. 
With decrease in temperature, eggs may be added, and in 
convalescence a gradual return to normal meals. The 
caloric system of feeding, though somewhat troublesome 
to carry out, is desirable, as then one can be sure that the 
fuel needs of the patient are being met. 

2. Drug or Specific Treatment. It is a sad fact that 
hitherto in modern medicine we are all too seldom able to 
treat the disease that confronts us. We can, and we do, 
treat the patient with the disease, but we treat him symp¬ 
tomatically, meeting indications as they arise, knowing 
full well that if we maintain his strength, keep his bowels 
and kidneys acting freely, and relieve him from the most 
burdensome of his symptoms, Nature will carry on the 
fight against the enemy. In the case of rheumatic fever, 
we possess, however, a remedy which seems to attack the 
disease directly, and which, while not producing results 
as brilliant as do antitoxin in diphtheria, and quinine in 
malaria, nevertheless deserves a high place among our 
weapons for fighting disease. This drug is salicylic acid. 


RHEUMATIC FEVER. 


27 


In order to obtain beneficial effects from this drug it 
must be administered in full doses. Salicylic acid itself 
may be given, or else its derivative, acetylsalicylic acid 
(aspirin), the latter being perhaps preferable, because 
less trying to the stomach. The dose of either drug in an 
adult is usually 15 to 20 grains every two hours. The ex¬ 
act manner in which salicylic acid acts upon the rheumatic 
poison is not known, but of its marked beneficial effect 
abundant clinical experience has given incontestable 
proof. The good results of the drug are seen upon all 
the symptoms—pain and swelling of joints, sweats, tem¬ 
perature, all abating under its proper use. Often sali¬ 
cylic acid is given credit for not producing the desired 
effect because the dosage has been too small. 

The limit of tolerance on the part of the patient must, 
however, not be overstepped. The following conditions 
may arise denoting that the patient can take no more of 
the drug: 

1. Ringing in the ears. 

2. Gastric disturbances: 

( a ) Nausea. 

( b ) Vomiting. 

3. Cardiac disturbances. Irregularities. 

4. Respiratory disturbances: 

(a) Dyspnea. 

(b) Sighing respiration. 

5. Cerebral symptoms: 

(a) Headache. 

( b ) Delirium. 

6 . Renal complications. Any variation from the nor¬ 
mal in the kidney functions. 

7. Hemorrhage. From bowels, bladder or under skin. 

8 . Skin involvement. Various rashes. 


28 CLINICAL MEDICINE FOR NURSES. 

Upon the appearance of any of these symptoms not 
accounted for by other evidences in the patient, the drug 
must be temporarily discontinued, and subsequently re¬ 
sumed in reduced dosage. 

In addition, alkalies in the form of the citrate and 
acetate of potash and the bicarbonate of soda are fre¬ 
quently given in full dosage, a good guide being the keep¬ 
ing of the urinary reaction alkaline. 

Symptomatic Treatment.. 

Pain. Rest is the best. Place pillows or bolsters under 
knees. Sometimes splints lightly put on will give relief. 

Cold. The ice-bag often eases pain. Especially is it 
valuable in pericardial pain, so frequent with beginning 
heart involvement. 

Heat is sometimes very effectual in allaying joint-pains. 
It is best applied in the form of hot fomentations, as 
follows: Two layers of flannel are soaked in very hot 
water, and wrung out of a wringer made of a crash 
towel. The flannel is applied singly to the joint. Ap¬ 
plications are repeated three or four times, at intervals of 
ten or fifteen minutes. The joints are then sponged with 
water at a temperature of 75°, and wrapped in dry flan¬ 
nel or wow-absorbent cotton. 

Oil of wintergreen applied to joints on cotton is often 
of great benefit, though the pungent and all-pervading 
odor may be objectionable. 

Blisters and the actual cautery over the joints may 
give great relief, and a fly-blister the size of a silver dol¬ 
lar over the pericardium is of great service in allaying 
pain in that region. 

Codeine or morphia in the usual dosage may be, and 
often are, necessary. 


RHEUMATIC FEVER. 


29 


Hyperpyrexia. Cold packs and cold sponges are indi¬ 
cated for temperatures of 104° F. or over, and should be 
given as in cases of typhoid fever ( q.v .). 

Convalescence. The patient recovering from an at¬ 
tack of rheumatic fever must be jealously guarded for a 
period longer than that required in convalescence from 
most acute infections. The reason for this is that the 
heart may be the seat of slight involvement which, if 
unwise liberties are allowed, may become more active, 
and give rise to an actual endocarditis. Consequently, 
many weeks of care and quiet are necessary, all exposure 
to cold and sudden changes of temperature must be 
avoided, and, if possible, when convalescence is once 
established, it is well to have the patient seek a climate 
that is sufficiently mild to enable him to live comfortably 
out of doors for a few weeks. Return to the normal 
activities of life must be very gradual, first consideration 
being given to the heart, which has been exposed to such 
likelihood of infection. 


CHAPTER V. 


PERICARDITIS. 

Pericarditis is inflammation of the pericardium, the 
membrane surrounding the heart. This membrane is 
composed of an outer coarse, fibrous layer, and an inner 
fine, serous layer. The pericardium surrounds the heart 
on all sides and, above, the beginning of the aorta and 
pulmonary artery. Below, the membrane is firmly at¬ 
tached to the diaphragm. 

The inner or serous portion of the pericardium is sub¬ 
divided into two layers; an outer one lying against the 
fibrous pericardium, and an inner one lying directly upon 
the heart muscle. Between these layers, which are in 
contact with one another, are found a few drops of fluid 
which act as a lubricant, as with each beat of the heart 
these two layers slide one upon the other. Inflammation, 
known as pericarditis, is practically limited to the serous 
portion of the pericardium, and does not involve the 
fibrous layer at all. 

Etiology. 

1. Rheumatic fever, the most common factor. 

2. Lobar pneumonia. 

3. Nephritis: 

(a) Acute. 

( b ) Chronic. 

4. Scarlet fever. 

5. Other infections. 

Pericarditis is almost always of infectious origin, and 
is brought about by germ action. Pericarditis is divided 
into two great classes: 

(30) 


PERICARDITIS. 


31 


1. Dry pericarditis. 

2. Pericarditis with effusion. 

Pathology. 

Dry Pericarditis. Congestion of the outer and inner 
serous layers of the pericardium. Exudation of serum, 
fibrin, leukocytes. 

Between the layers a meshwork of fibrin is formed 
which prevents the two surfaces of membrane from work¬ 
ing smoothly, one against the other. This meshwork is 
frequently found to contain bacteria. The heart muscle, 
which lies next to the inner layer of the membrane, is 
secondarily affected, and the individual muscle fibres, 
when examined under the microscope, may show degen¬ 
erative changes. 

Pericarditis with Effusion. Instead of the formation 
of a meshwork of fibrin, with but a small amount of 
serum, in this variety of pericarditis the exudation of 
serum (fluid) is the main features The exudate is very 
abundant, and in extreme cases may amount to as much 
as a quart. The nature of the fluid given off from the 
surfaces of the membrane depends upon the nature of the 
infecting germ. It may be: 

1. Serous—a clear, yellowish fluid. 

2. Purulent—cloudy, or yellow, from the presence 

of pus. 

3. Hemorrhagic—bloody. 

Symptoms. Pericarditis rarely appears as a primary 
disease. It usually makes its appearance as a complica¬ 
tion of some pre-existing infectious disease. Hence, be¬ 
cause of the existence of another malady, those symp¬ 
toms due particularly to pericarditis are apt to be masked. 
For instance, if in the course of rheumatic fever there 
is a rise in temperature, without the involvement of addi- 


32 


CLINICAL MEDICINE FOR NURSES. 


tional joints, or without the onset of delirium or other 
nervous symptoms, pericarditis should be thought of as a 
possibility. The following symptoms are those most 
characteristic of 

A. Dry Pericarditis. 

1. Pain in the region of the heart, or in the epigas¬ 
trium. It may at times radiate to the front and sides of 
the chest. Pain is due to the abnormal friction between 
the layers of the pericardium, arising because of the pres¬ 
ence of the fibrin meshwork. It may be sharp or dull, 
and is usually continuous. If the pain suddenly ceases 
while the temperature fails to drop, it is a sign that effu¬ 
sion has set in. Effusion stops the pain by mechanically 
separating the layers of the pericardial membrane, so that 
they no longer rub against each other. 

2. Cough. May or may not be present. If present, 
is frequent, and of the dry, hacking variety. 

3. Pulse. Invariably rapid, 120 to 140. Soft and com¬ 
pressible. Regular until the heart muscle is affected, 
when irregularities are apt to occur. 

4. Respiration. Rapid and shallow. 

5. Temperature. Usually raised moderately (100° to 
102 °), but in no> way characteristic or to be relied upon, 
as it is affected by the fever arising from the primary dis¬ 
ease, of which pericarditis is a complication. 

6 . Sleep. Disturbed because of pain and general nerv¬ 
ous irritability. 

Course of the Disease. One to several weeks. The 
inflammation may wholly disappear and complete recov¬ 
ery ensue. The inflammation may extend to the heart 
muscle, and give rise to myocarditis. Effusion may ap¬ 
pear. The outlook in pericarditis is always grave, much 
depending upon the nature of the primary disease. 


PERICARDITIS. 


33 


B. Pericarditis with Effusion. In the early stages, the 
symptoms are the same as those of the dry variety ( q.v .). 
Later, the symptoms are those caused by the accumula¬ 
tion of fluid in the pericardial sac, causing pressure 
on the heart. 

1. Cessation of pain. 

2. Fever and cough usually persist. 

3. Facial pallor and anxious look. There may be 
slight cyanosis. 

4. Pulse: Small, rapid, and of low tension. It be¬ 
comes irregular when the effusion is large and has per¬ 
sisted for some time. This is a bad sign, as it indicates 
failure of the heart muscle. If, however, owing to some 
pre-existing heart disease, the pulse has been irregular 
right along, the outlook is not so grave. The pressure 
of the fluid on the heart hinders the entrance of blood 
into the heart more than it does the exit of blood from 
the heart (for blood coming to the heart is under very 
slight pressure as compared with that of blood leaving 
the heart) ; hence, there is dilatation of the small veins 
of the skin. 

5. Respiration. Rapid and shallow, and in large effu¬ 
sions much embarrassed, both because of pressure of 
fluid on the heart and because of pressure on the ad¬ 
jacent lung, especially the left lower lobe. 

6 . Insomnia. Marked and intractable. Due to con¬ 
gestion of the brain by the damming back of the blood, 
and also to shortness of breath. 

7. The abdomen may be distended with gas, due to 
congestion in the portal system of veins. There may be 
constipation or small, frequent, watery stools, because of 
the passage of serum from the greatly congested blood¬ 
vessels into the intestines. 


3 


34 


CLINICAL MEDICINE FOR NURSES. 


Course of the Disease. Two weeks to two months. 
The effusion may become absorbed in from two to four 
weeks. More often, however, it shows a tendency to 
remain. Partial absorption may be followed by more 
effusion. The outlook is always very grave. 

Treatment. 

Dry Pericarditis. There is no specific method of 
treatment that can be used. The patient must be care^ 
fully watched, and every effort made to help Nature. 
Treatment that has been instituted for the primary dis¬ 
ease, whatever that may be, will, of course, be continued. 
In most cases, absolute and prolonged rest in bed is indi¬ 
cated. Most physicians approve of counterirritation 
over the heart in the shape of: 

1. Heat (hot water bags, hot bottles, mustard plas¬ 

ter, iodine). 

2. Fly-blisters. 

3. Cold. Often more effective than heat. Best ap¬ 

plied by means of the ice-bag or cold-water 
coil. 

Other treatment is symptomatic. Cough, insomnia, 
fever, etc., must be met and combated by the usual meth¬ 
ods. Frequently, moderate doses of codeine or morphia 
are given to relieve, pain and give much needed rest. 

For rapid and violent heart action, the ice-bag gives 
the best results. Heart stimulants are usually not needed, 
especially at first, as the rapid heart action is due to irri¬ 
tation of the heart, and not to weakness of that organ. 
The bowels should, of course, be kept well open, and the 
diet should be bland and easily digestible, consisting in the 
main of milk, eggs, chicken, raw oysters, birds, toast, etc. 
It should not be bulky, and should be given frequently 
and in small amounts. 


PERICARDITIS. 


35 


Pericarditis with Effusion. Two methods of treatment 
are available, the object of each being, of course, to get 
rid of the effusion: 

1. Elimination by catharsis , the object of this method 
being to give such drugs as will abstract fluid from the 
tissues, and therefore indirectly remove the fluid that has 
collected in the pericardium. Saline cathartics are those 
most employed. 

2. Tapping. (Paracentesis pericardise). 

This is called for by: 

1. Marked shortness of breath. 

2. Marked cyanosis. 

3. Marked rapidity and weakness of pulse. 

The location for tapping the pericardium is the fifth 
left intercostal space, very near the sternum, or else one 
inch from that bone, in order to avoid the internal mam¬ 
mary artery. 


CHAPTER VI. 


ENDOCARDITIS (ACUTE SIMPLE AND 
MALIGNANT). 

Endocarditis is the name given to inflammation of the 
endocardium or lining membrane of the heart. 

Cases of endocarditis can be classified as follows: 

1. Sirpple endocarditis. 

(a) Acute. 

( b ) Chronic. 

2. Malignant or ulcerative endocarditis. 

Etiology. In the vast majority of cases simple acute 

endocarditis is of bacterial origin. Malignant endocar¬ 
ditis is invariably caused by some micro-organism. Al¬ 
though the causative germs of some of the diseases most 
frequently giving rise to endocarditis have not as yet been 
discovered (rheumatic fever, scarlet fever, measles), still 
there is every reason to believe that these diseases are of 
microbic origin. 

The following diseases most frequently give rise to 
simple endocarditis: 

Rheumatic fever (by far the most important). 

Tonsillitis. 

Chorea (St. Vitus’ dance). 

Scarlet fever. 

Measles. 

The following diseases most frequently give rise to 
malignant endocarditis: 

Septicemia. 

Pyaemia. 

( 36 ) 


ENDOCARDITIS. 


37 


Fresh bacterial invasions. 

Pneumonia. 

Gonorrhea. 

Pathology. The following changes take place in the 
endocardium, which normally is a smooth, shiny, glisten¬ 
ing membrane: 

1. Cloudiness of the membrane. 

2. Thickening and some edema. 

3. Laceration. 

4. An eroded surface, necrotic from the the action of 
bacteria and their toxins, covered with a deposit of fibrin 
which forms a warty cauliflower-like mass, yellowish or 
reddish, the so-called “vegetation.” This may occur any¬ 
where on the endocardium, but most frequently on the 
cusps of the valves at or near their free border. 

5. Repair. Granulation tissue replaces the fibrin, and 
cicatricial contraction takes place, resulting very fre¬ 
quently in permanent damage to the valve. 

In the malignant variety of endocarditis emboli may 
become detached from the vegetation at any time, and 
float ofif in the blood current. These emboli invariably 
contain bacteria, and are known as septic emboli. Upon 
their lodgement in any portion of the* body they form 
abscesses, which are known as metastatic abscesses. 

Symptoms. 

Simple Acute Endocarditis. As already mentioned, 
this disease is almost never a primary affection, but oc¬ 
curs as a complication of some pre-existing ailment. 
Hence, as in the case of pericarditis, the symptoms are 
apt to be masked by those of the primary disease. 

As rheumatic fever is by far the most common cause 
of simple endocarditis, this disease is selected as the type 
upon which to base a detailed recital of the symptoms. 


38 


CLINICAL MEDICINE FOR NURSES. 



B 



Fig. 3.—Endocarditic lesions. A, ulcerative endocarditis 
with perforation of one of the aortic cusps. B, healed chronic 
endocarditis of the mitral valve. (Hirschfelder, Diseases of 
the Heart and Aorta.) 




ENDOCARDITIS. 


39 


With the onset of an acute endocarditis in the course 
of rheumatic fever, the temperature rises without the in¬ 
volvement of any new joints. The rise is not usually 
great, and has no distinctive characteristics, but the fever 
is frankly higher than has previously been the case. 

Pericardial pain, usually constant and dull, may occur. 
The patient may experience a sense of oppression in the 
chest, or may complain of palpitation (consciousness of 
the heart-beat). Subjective dyspnea may be present. 
By this is meant a feeling on the part of the patient of 
shortness of breath, amounting sometimes to actual air- 
hunger, in the absence of any discoverable signs or symp¬ 
toms sufficient to give rise to this feeling. It is due to 
the liberation and absorption of toxins. 

A rise in the pulse-rate is frequently noticed, but save 
for this there is often found no noticeable change in the 
circulation. In some cases, fortunately rare, the onset of 
simple endocarditis is marked by the symptoms of an 
intense general infection, with profuse sweating, bad 
pulse, etc. 

Course and Prognosis. Simple endocarditis usually 
lasts several weeks, though it is impossible to tell exactly 
when the infectious process has spent itself. The out¬ 
look is always grave. 

Three conditions may result: 

1. Death; not common; though if the patient is al¬ 
ready greatly enfeebled by the pre-existing disease, he 
may be unable to withstand the added endocardial infec¬ 
tion. 

2. Recovery; may and does occur, but unfortunately 
not often. 

3. Conversion of acute endocarditis into chronic endo¬ 
carditis. This happens in the vast majority of instances. 


40 


CLINICAL MEDICINE FOR NURSES. 


The patient is able to withstand the infection, but the 
cicatricial contraction taking place in the process of re¬ 
pair shortens the valve cusp and permanently damages 
it (see Fig. 3B). Leakage then occurs, and the individ¬ 
ual is the victim of chronic valvular heart disease. 

Symptoms of Malignant Endocarditis. In consider¬ 
ing the symptoms of this condition it is best to bear in 
mind that malignant endocarditis is simply general sepsis 
plus heart disease . Many cases occur in which no dis¬ 
order of the heart can be discovered during life, and 
often the disease is diagnosed at first as typhoid fever. 

The symptoms are many, varied, and misleading. In 
the main, they are those of general sepsis: 

Irregular fever. 

Sweats-chills. 

Prostration. 

Marked anemia. 

Dry brown tongue. 

Anorexia. 

Abdominal distention. 

Low muttering delirium. 

Enlargement of the spleen. 

Sometimes symptoms may occur referable to the heart 
itself, when of course, recognition of the condition be¬ 
comes less difficult. As a result of the septic emboli, ab¬ 
scesses may occur in any part of the body. 

Duration and Prognosis. Malignant endocarditis 
runs its course in a few weeks or at most two or three 
months. The outlook is hopeless. ' 

Treatment. 

Acute Simple Endocarditis. First in importance is 
rest in bed, in the recumbent position. The use of the 
bed-pan should be insisted upon. Rest must be main- 


ENDOCARDITIS. 


41 


tained for many weeks or months in order to give the 
heart as little labor as possible. Patients generally find 
the confinement in bed long after all symptoms have dis¬ 
appeared as very irksome, and one of the reasons why so 
many cases of acute endocarditis go over into the chronic 
form is that patients refuse to submit to rest for a suffi¬ 
cient length of time. 

The diet should be light, but nutritious. The patient’s 
taste can be largely catered to. Attention must, of course, 
be given to the bowels and kidneys, which should be 
kept active. 

An ice-bag over the heart is of value in quieting its 
action, and thus tending to relieve it of some of its work. 

Drugs are not of much value. In acute endocarditis 
cardiac stimulants are not looked upon generally with 
favor, as the heart is irritated, not depressed, and does 
not require urging to do its work. Sometimes, if the 
heart shows sign of failing, stimulation is of course in 
order. Pain must be met by sedatives, such as codeine 
and often morphia. 

Malignant Endocarditis. Little can be done for this 
distressing condition. The treatment is mainly sympto¬ 
matic, and the general management is in no way charac¬ 
teristic. If the organism causing the infection can be 
discovered, treatment by means of a vaccine made from 
that organism (an autogenous vaccine) may prove of 
some aid. 


CHAPTER VII. 


ENDOCARDITIS (CHRONIC). 

Etiology. Chronic endocarditis is frequently a sequel 
of acute endocarditis, and is, therefore, dependent upon 
the same causative factors as that disease (q-v.). It may 
be chronic from the start, or may be the result of a gen¬ 
eral sclerotic or fibrosing process throughout the body 
brought about by: 

O) Age. 

( b ) Arteriosclerosis. 

(c) Syphilis. 

( d) Alcoholism. 

Nature of the Process. The valves of the heart are 
the structures that are damaged. Endocarditis, whether 
acute or chronic, practically always affects the left side 
of the heart; hence the valves that are the seat of the 
disease are either the mitral or the aortic. The cusps of 
the valves are the seat of a chronic inflammatory process 
that results in a thickening and contraction of the valve 
flaps. As a result one of two conditions may arise: 

1. The valve cannot close completely, so that some 
blood leaks back through it. This is called regurgitation. 

2. The valve cannot open sufficiently to let the requi¬ 
site amount of blood pass through it. This is called 
stenosis. 

There are, then, four varieties of valvular disease that 
commonly occur as a result of chronic endocarditis. 
These are in their order of frequency: 

(a) Mitral regurgitation. 

( b ) Mitral stenosis. 

(42) 


ENDOCARDITIS (CHRONIC). 


43 


(c) Aortic regurgitation. 

( d ) Aortic stenosis. 

A few words concerning each variety will be of service: 

(a) Mitral Regurgitation. With each ventricular sys¬ 
tole the mitral valve should close so that all the blood in 
the ventricle can go into the aorta. When the mitral 
valve is deficient, or leaky, with each beat of the heart 
a portion of the blood in the ventricle is sent back through 
the mitral opening into the left auricle. 

( b ) Mitral Stenosis. When the mitral valve cannot 
open sufficiently to allow the passage of the requisite 
amount of blood, necessarily a portion of the blood is 
dammed back in the left auricle and into the four pul¬ 
monary veins, and, as the full amount of blood cannot 
reach the left ventricle, that chamber has an insufficient 
amount to deliver into the aorta at each ventricular sys¬ 
tole. 

(c) Aortic Regurgitation . At the completion of each 
ventricular systole, the ventricle is empty and the blood 
it contained is in the aorta. As soon as ventricular sys¬ 
tole is over, the aortic semilunar valves should close and 
prevent any blood from flowing back into the left ven¬ 
tricle. When the aortic valves are leaky, some blood 
flows back into the ventricle during each ventricular 
diastole, thus preventing the requisite amount of blood 
from being delivered to the tissues with each beat of the 
heart. 

( d ) Aortic Stenosis. When the aortic valves cannot 
open sufficiently to admit the requisite amount of blood 
that should flow past with each ventricular systole, neces¬ 
sarily a portion of the blood will be dammed back in the 
left ventricle and an insufficient amount of blood deliv¬ 
ered to the tissues. 


44 


CLINICAL MEDICINE FOR NURSES. 


The Phenomenon of Compensation. The heart is the 
most adaptable organ in the body. Were it not for its 
adaptability it could never withstand the sudden and un¬ 
expected strains thrown upon it at any and all times. 
For purposes of general discussion, the four valvular dis¬ 
eases under consideration can be grouped together. 
Each has a few special symptoms peculiar to it, and each 
is diagnosed by special physical signs discovered upon 
examination, but all four have this in common: a dis¬ 
order in the mechanics of the circulation. 

The changes in the valves do not take place overnight, 
but gradually and insidiously. Therefore, the heart has 
an opportunity to accommodate itself to changing condi¬ 
tions, and this it does marvelously well. 

When blood is leaking back through any valve, or pre¬ 
vented from flowing through any valve in a sufficient 
amount, the heart, in order to maintain the mechanics of 
the circulation, must obviously do two things: 

1. Work faster—increased beat-rate per minute. 

2. Work harder—increased power of individual con¬ 
tractions. 

The combination of these two factors constitutes what 
is known as cardiac compensation. The heart responds 
to the increased demands made upon it, and instead of 
the pulse-rate at rest being about 72 to the minute, the 
number of beats reaches 85 to 90, or even more. To¬ 
gether with this, each contraction of the heart is stronger 
and more powerful than is normally necessary. Just as 
exercise of any muscle or group of muscles causes an 
increase in size, so increase in the exercise of the heart 
causes an increase in the size of its individual muscle- 
fibres and in the thickness of the heart walls. Muscle- 
fibres are increased in size, and new fibres make their 
appearance. This change is known as hypertrophy f and 


ENDOCARDITIS (CHRONIC). 


45 


must be sharply differentiated from dilatation (presently 
to be mentioned) a condition in which the size of the 
heart is also increased. 

Thus, by the combination of the two factors mentioned, 
the heart makes up for the leakage of blood through its 
damaged valve or valves, and, by driving blood more fre¬ 
quently into the aorta, maintains the circulatory balance. 
As long as this condition exists, compensation is estab¬ 
lished, and the patient suffers from no symptoms. 

But the situation can well be likened to whipping a 
horse to make him run faster. For a while he responds 
with increased effort and increased speed, but he tires 
more quickly because of the excessive rate at which he is 
running, and because of the extra output of physical 
strength. So- it is with the heart. For a time—months 
or years—the fast pace is maintained. The time in¬ 
evitably comes, however, when the strain can be no 
longer endured, and the heart begins to show signs of 
fatigue. The muscle-fibres no longer contract as strongly. 
They stretch, and show signs of degeneration. The heart 
chambers become larger through this stretching, and 
through loss of “tone” of their walls. Then it is that 
the condition known as dilatation sets in, producing an 
increase in the size of the heart, but this time not from 
strength, as in hypertrophy, hut from weakness and be¬ 
ginning exhaustion. As soon as this happens the me¬ 
chanics of the circulation begin to fail (for the body is 
inexorable, and must have its proper quota of blood at 
all times), symptoms make their appearance, and com¬ 
pensation is said to be failing. 

Finally, when this state of things has progressed still 
further, when it is all the heart can do to maintain 
sufficient circulation to support life, and when on all 


46 


CLINICAL MEDICINE FOR NURSES. 


sides the symptoms of circulatory failure are in evi¬ 
dence, compensation is said to be lost. 

The Course of the Symptoms in Chronic Endocar¬ 
ditis. Practically all symptoms occurring, in chronic 
valvular disease are of mechanical origin, i.e., arise 
from a disturbance in the normal blood-flow. They have 
a common cause, which can be summed up in three 
words: chronic passive congestion. As an illustration 
of their occurrence, may be selected a case of mitral re¬ 
gurgitation, the most common valvular disease, with 
decided failure of compensation. The description, with 
a few minor alterations, will fit any of the other three 
valvular lesions under discussion. 

In mitral regurgitation the blood leaks back from the 
left ventricle through the mitral orifice into the left 
auricle, and a general damming back of the blood cur¬ 
rent, and a slowing in its rate of flow, is felt in the pul¬ 
monary veins and in the vessels of the lungs. This gives 
rise to a chronic passive congestion of the lungs, which 
causes a deficient aeration of the blood, resulting in (1) 
dyspnea and (2) cyanosis; as a result of this chronic pas¬ 
sive congestion there is an excess of mucus in the air 
alveoli and bronchial tubes, causing irritation, and re¬ 
sulting in (3) cough and (4) expectoration. The dam¬ 
ming back of the blood is next apparent in the right side 
of the heart, which, while perfectly sound, is not able to 
force the blood onward through the lungs because of the 
increased resistance encountered. As a result, there is 
slowing of the blood current, and a relative stagnation in 
the systemic veins, resulting in a chronic passive con¬ 
gestion of the mucous membrane of the stomach and 
causing (5) loss of appetite, (6) nausea, and (7) vomit¬ 
ing. There is also a chronic passive congestion of the 


ENDOCARDITIS (CHRONIC). 


47 


intestines, resulting in (8) tympanites, and of the colon 
and rectum, showing itself by (9) constipation and (10) 
hemorrhoids. The state of chronic passive congestion 
in the entire body causes an escape of serum from the 
blood-vessels, resulting in (11) edema. When this con¬ 
dition becomes more pronounced, as a result of chronic 
passive congestion, fluid appears in the abdominal cavity, 
and (12) ascites is present. The other serous mem¬ 
branes of the body (the pleura and pericardium) may be 
similarly afifected, resulting in the conditions known as 
(13) hydrothorax and (14) hydropericardium. Even¬ 
tually, when, as a result of universal chronic passive con¬ 
gestion, the serous cavities contain fluid, and edema is 
general, the condition known as (15) general anasarca is 
present. Chronic passive congestion in the brain gives rise 
to symptoms of (16) headache, (17) sleeplessness, (18) 
dizziness, (19) vertigo, and sometimes to (20) faintness 
and (21) periods of unconsciousness. Chronic passive 
congestion of the kidneys causes (22) scanty high- 
colored urine. Thus we see that practically all the symp¬ 
toms of chronic valvular disease, with the exception 
of (23) palpitation and (24) rapid heart action, can be 
traced to the gradual damming back of the blood 
throughout the entire circulatory system, and to the re¬ 
sulting universal chronic passive congestion . 

It not infrequently happens that more than one val¬ 
vular lesion exists, and also very often, as compensation 
fails, a sound valve will become leaky—not because it has 
become diseased, but because, owing to the great dilata¬ 
tion of the heart, the ring to which the valve cusps or 
flaps are attached becomes stretched, and the valve cusps, 
though in proper working order, are not able to meet, and 
thus close the opening they are set to guard. A valve 


48 


CLINICAL MEDICINE FOR NURSES. 


that, sound itself, does not functionate properly because 
of dilatation of the ring to which the cusps are attached, 
is known as “relatively insufficient/’ 

The pulse is usually regular while compensation is 
maintained, but as it fails, irregularity begins and be¬ 
comes more and more pronounced, until, at the end, the 
heart often beats in an absolutely irregular manner, de¬ 
void of rhythm, auricles and ventricles beating when 
they wish, with no relation one to the other, and the con¬ 
dition of “delirium cordis” (delirium of the heart) is 
present. 

In mitral stenosis the pulse is very small, i.e., the ves¬ 
sel seems to make a small excursion against the finger, 
because of the relatively small amount of blood forced 
into the aorta. In aortic regurgitation, on the other hand, 
the full amount of blood is thrown into the aorta, but 
some leaks back into the ventricle; therefore, the pulse 
is very large, i.e., the artery seems to be filled to the limit, 
and then practically emptied. This is known as the Cor¬ 
rigan or water-hammer pulse. Again, in aortic regur¬ 
gitation, because of the rapid alternate filling and empty¬ 
ing of the vessels (due to the leakage back from the aorta 
into the left ventricle), if the skin on the forehead is 
rubbed with a towel so as to make it red, an alternate 
flushing and paling can be seen, the flushing correspond¬ 
ing with each beat of the heart. This is known as the 
“capillary pulse.” 

Edema is at first slight, usually noticed in the feet, 
ankles, and legs, and more marked if the limbs are 
allowed to hang down. With progressive failure of com¬ 
pensation, however, it grows steadily more extensive. 

Dyspnea is complained of early in failure of compen¬ 
sation, and, in cases that do not rally, is a constant and 


ENDOCARDITIS (CHRONIC). 49 

distressing symptom. At the last it dominates the scene, 
becoming extremely urgent, necessitating the sitting pos¬ 
ture to make it bearable, and causing the “getting of the 
breath” to be the one absorbing idea of the patient. 

Cough and expectoration are to some extent present 
throughout the course of failing compensation. As the 
end approaches, the patient is exhausted by the cough, 
and too weak to raise the sputum. The terminal phase 
is frequently edema of the lungs, the patient practically 
drowning in his own secretions. 

Sleeplessness is a great torment, and is often most re¬ 
sistant to all manner of treatment. In addition to the 
cerebral congestion which causes it, must be mentioned 
other symptoms, such as dyspnea and cough which add 
to its severity. 

Auricular Fibrillation: Auricular fibrillation is a con¬ 
dition in which the auricles are in a continuous state of 
tremulous movement, and with no coordination, a wave 
of contraction apparently sweeping over their muscular 
walls. 

Impulses to ventricular contraction are nervous in 
origin and proceed from a small node of nerve fibres 
situated at the junction of the superior vena cava and the 
right auricle and known as the sino-auricular node, or 
“pace-maker” of the heart. These impulses are carried 
to a bundle of nerve fibres running from auricles to ven¬ 
tricles and called the “auriculo-ventricular bundle” or the 
“bundle of His” which runs into the septum or wall be¬ 
tween the two ventricles and divides into two branches, 
one going to the right ventricle and the other to the left. 
Under normal conditions impulses come down from the 
sino-auricular node through the auricles and are trans¬ 
mitted to the ventricles in a regular rhythmic manner. 


4 


50 


CLINICAL MEDICINE FOR NURSES. 


When, however, the auricles are “fibrillating” the sino- 
auricular node or pace-maker has ceased to function, for 
more impulses to contraction are delivered to the ven¬ 
tricular muscle than it can take care of. The result is 
that the ventricles try to contract in response to the over¬ 
frequent stimulations and cannot keep pace with them. 
There is, therefore, complete ventricular arrhythmia, the 
contractions varying both in rapidity and in power. The 
'pulse is absolutely irregular and all ventricular contrac¬ 
tions cannot be felt at the wrist, as can easily be appreci¬ 
ated if the radial pulse is felt with one hand, while the 
other is placed over the heart. Not only will it be per¬ 
ceived that all ventricular contractions are not felt at the 
wrist but it will further be noted by the hand over the 
heart that the ventricular contractions vary to the utmost, 
not only in rhythm but in strength, some being very 
forcible and others barely perceptible. Naturally the 
mechanics of the circulation are markedly interfered with 
and all symptoms of failing compensation ensue even in 
the absence of any definite valvular defect. A positive 
diagnosis of auricular fibrillation can only be made from 
tracings obtained by means of the electrocardiogram, but 
clinically, marked or complete loss of regularity in the 
ventricular contractions, coupled with a very rapid heart 
rate, is presumptive evidence that the auricles are fibril¬ 
lating. This condition occurs often in conjunction with 
cases of valvular heart disease and it is for this reason 
that it has here been referred to. 

Prognosis. The outlook in cases of chronic valvular 
heart disease and in cases of auricular fibrillation is al¬ 
ways grave. The condition is incurable, but many in¬ 
dividuals by the exercise of care and moderation can live 
long and happy lives. Unfortunately, the majority have 


ENDOCARDITIS (CHRONIC). 


51' 


to work, and work hard, to live, and the heart cannot 
stand the inevitable strain. They can be patched up— 
once, twice, thrice—but sooner or later another failure of 
compensation ensues that proves fatal. Generally speak¬ 
ing, the outlook is better in the well-to-do than in the 
poor, in the exemplary than in the dissipated, and in 
mitral rather than in aortic disease. Prognosis also de¬ 
pends largely upon the faithfulness with which the patient 
carries out instructions, not alone as to medicines, but 
also as to mode of life and the avoidance of excesses of 
all kinds. The outlook is also largely affected by condi¬ 
tions of a technical nature residing within the heart, 
which only a physician of experience can estimate and 
appreciate. 

Treatment. The nurse will not be called upon, 
save in rare instances, to care for patients in whoqj, com¬ 
pensation is fully established. Such cases form a part of 
every physician’s office practice, and do not concern us 
at this time. The nurse is called in when compensation is 
failing or lost. It is quite impossible to describe the man¬ 
agement of these cases, ranging as they do from mild 
failure of compensation to complete circulatory insuffici¬ 
ency. A moderately severe case must be taken as an 
example. 

In the presence of loss of compensation, all the condi¬ 
tions enumerated above present, in the main, one and the 
same picture, that of heart failure. 

Treatment of Heart Failure. There are three main 
divisions in the treatment of heart failure, and several 
subdivisions. The main divisions are: 

1. Rest. 

2. Morphia. 

3. Digitalis. 


52 


CLINICAL MEDICINE FOR NURSES. 


1. Rest. Perfect rest can, of course, never be given to 
the heart, but relative rest can, and is of the utmost im¬ 
portance. Bed is absolutely essential and the patient must 
make no effort which can possibly be prevented. Theo¬ 
retically the recumbent position is the best, for then the 
heart does not have to pump blood “up hill,” but practi¬ 
cally the position of greatest comfort to the patient is the 
one for him to assume, as he naturally chooses that in 
which effort is least. Some patients at first will have to 
sit almost upright and cases have been frequently seen 
where greater comfort was obtained in a large armchair 
than in bed, at least until compensation had been some¬ 
what re-established. The main point is the ease and com¬ 
fort of the patient. This must always be borne in mind. 
Eventually, with the favorable progress of the case, the 
patient,will become able to lie flat and with the ability to 
do this in comfort will unfailingly come willingness to 
go to bed. The bed-pan and bed urinal must then be in¬ 
sisted upon and the patient fed so as to eliminate all 
sources of effort. The duration of bed rest is, of course, 
to be determined by the physician. It will usually last 
several weeks and, as in the case of acute endocarditis, is 
frequently given up too soon because of the inability or 
disinclination of the patient to further submit to it. 

2. Morphia. In the moderately advanced and far ad¬ 
vanced stages of heart failure there is no drug that tides 
the patient over and adds more to his comfort than mor¬ 
phia. The advantages are manifold: 

(a) Relief of anxiety. 

( b ) Relief of dyspnea. 

(c) Securing of sleep. 

(d) Relief of exhausting cough. 

( e ) Giving the heart time to “catch up with itself.” 


ENDOCARDITIS (CHRONIC). 


53 


The dosage, of course, must be individualized, but as 
a general rule it is wise to give fairly full doses for a 
short time, one or two days, until digitalis has had time 
to exert its influence upon the heart. By full doses no 
definite amount of morphia is meant, but enough to se¬ 
cure the desired effect. Of course, not enough should be 
given to cause stupor or to thicken the pulmonary secre¬ 
tions, but it is a mistake to quibble about an extra eighth of 
a grain when rest, both physical and mental, are so es¬ 
sential to the patient. In the author’s experience much 
more harm has resulted from the withholding of morphia 
in cases of heart failure than from its prompt and ade¬ 
quate administration. 

3. Digitalis. Digitalis comes to its own in the treat¬ 
ment of heart failure, and especially in cases due to pure 
auricular fibrillation, or in those cases in which fibrillation 
develops in the presence of a valvular lesion. Digitalis 
works such wonders in cases of auricular fibrillation by 
cutting off a large number of contractile impulses coming 
from the sino-auricular node along the bundle of His for 
distribution to the ventricles. So many of these are cut 
off that the ventricles are given time to catch up with 
themselves as it were, and thus to contract more strongly 
and in a more rhythmical manner. In addition, digitalis 
tends to slow the heart rate by stimulation of the vagus 
nerve which actes as a brake on the heart rate. Further¬ 
more, digitalis stimulates heart-muscle tone, by which is 
meant the average contractile state in which muscle finds 
itself even when not working. For example, it is well 
known that fatigue stretches muscle fibres. Let us as¬ 
sume for argument’s sake that normally a heart muscle 
fibre is half an inch in length. As a result of decompensa¬ 
tion and consequent fatigue each individual muscle fibre 


54 


CLINICAL MEDICINE FOR NURSES. 


loses some of its tone, i.e., it stretches to, let us say, % of 
an inch. Under the influence of digitalis each muscle 
fibre will regain some of this lost tone, shortening again 
to % or even % 6 of an inch. It can readily be seen how 
this shortening of countless muscle fibres will reduce the 
size of the chambers of the heart by a universal shrinking 
of their walls. 

To summarize briefly: 

(1) Digitalis cuts off a number of contractile impulses 
coming from auricles to ventricles in cases of auricular 
fibrillation. 

(2) In so doing it lessens rate of contraction of 
ventricles. 

(3) Digitalis stimulates the vagus nerve, thus prolong¬ 
ing diastole or the rest period of the heart. 

(4) Digitalis betters the tone of the heart muscle, thus 
both increasing its strength and reducing dilatation. 

Asa result: A smaller chamber, enclosed in stronger 
walls, delivers a more adequate amount of blood with 
greater strength at a slower rate and in a more rhythmic 
manner, thereby in every way improving the mechanics 
of the circulation and tending to overcome the symptoms 
of decompensation by a better blood-supply. 

The Dosage of Digitalis: 

Modern methods of research have shown that former 
doses of digitalis were far too small. Eventually, the 
same result was obtained as is now reached with large 
doses, but its accomplishment took from a week to ten 
days instead of from forty-eight to seventy-two hours. 
In mild cases of decompensation this did not matter much; 
in urgent cases it mattered a great deal. Eggleston and 
Hatcher have standardized digitalis by means of what is 
known as the “cat unit.” This “cat unit” is the “minimal 


ENDOCARDITIS (CHRONIC). 


55 


fatal dose of dry drug in milligrams that will kill one 
kilogram (2.2 pounds) of cat when injected intravenously 
and continuously.” Standard preparations now assay at 
approximately 100 mg. to the cat unit. The tincture, 
which is the preparation now most used, would therefore 
assay at 1 cat unit per cubic centimeter. For full digi¬ 
talization of the heart it has been found that 0.15 cat 
units or 2 minims of the tincture per pound of body 
weight are necessary. Thus, an individual weighing 150 
pounds would require 300 minims (150 X 2) or 22.5 c.c. 
(150 X 0.15) of the tincture of digitalis. According to 
the Eggleston method, in urgent cases from one-third to 
one-half the total amount is administered at the first dose. 
In our hypothetical case from 100 to' 150 minims or from 
7 to 11 c.c. After six hours % to % the total amount is 
administered and after another six hours .% to %. If 
more digitalis is needed, ! /i 0 of the full dosage is given 
every six hours until full digitalization is obtained. For 
less urgent cases % the full dose is given every six hours 
for two doses, and thereafter y i0 to % the full dosage' 
every six hours until the proper amount has been taken. 
If the patient has taken digitalis within ten days, more 
than seventy-five per cent, of the total dosage should not 
be given. 

There are three cardinal symptoms which denote full 
digitalization and call for discontinuance of the drug. 

1. Nausea and vomiting. 

2. Fall of heart rate (not pulse rate) to sixty beats per 
minute. 

3. Appearance of pulse or heart irregularity if not 
previously present. These rules for digitalis dosage have 
been rather dogmatically set down, simply to show clearly 
what is meant .by the modern large-dose method and how 


56 


CLINICAL MEDICINE FOR NURSES. 


it is applied. One of the values of the method consists 
in its extreme elasticity and every physician will vary it 
somewhat in almost every case. The general principle 
must, however, be clearly understood. By its use prompt 
and full digitalization are secured in a minimum of time 
and better effects are obtained than by the old dosage of 
“10 to 15 minims every four hours.” 

One point is of importance particularly as regards the 
nurse, as it is she who will administer the dose. The 
minim and the drop are not identical by any means, the 
average drop being usually smaller than the minim. Pratt 
reports a case where 40 “drops” were found equal to but 
15 “minims.” Hence an ordinary dropper should never be 
used for measuring the dose of tincture of digitalis. A 
minim droper should be employed, or if that is not avail¬ 
able the dose can be accurately measured in a hypodermic 
syringe graduated in minims. The measuring of dram 
doses of tincture of digitalis in graduated medicine glasses 
.should be prohibited as this method is bound to be far 
from accurate. When dealing with large doses of a 
powerful drug, accuracy in measurement is imperative. 
In the event of other drugs being necessary, the author 
has seen the greatest benefit from camphor in oil (9 to 
15 grains every three hours for a few doses) and aromatic 
spirits of ammonia, the former being given always hypo¬ 
dermically and the latter by mouth in dram doses every 
three to four hours or else almost constantly by inhala¬ 
tion. Camphor is hardly regarded as a heart stimulant 
and it is well known that both its action and that of 
ammonia are very transient but in urgent cases they help 
mainly by stimulating respiration. The ordinary text¬ 
book dose of camphor in oil (3 grains) is absolutely 
worthless. 


ENDOCARDITIS (CHRONIC). 


57 


4. Symptomatic Treatment. Many special symptoms 
arise that necessitate attention. Dyspnea is often greatly 
helped by digitalis, but, until that drug has had time to 
show its full effect, morphia may be necessary. In the 
terminal stages of valvular disease morphia affords the 
patient the greatest relief. 

Edema will often disappear to a surprising extent under 
digitalis, due in all probability to improvement in the cir¬ 
culation and not to any specifically diuretic action of the 
drug, but when this symptom is very marked, free pur¬ 
gation with salines in a manner similar to that described 
in the chapter on nephritis, is often resorted to. Ascites 
and hydrothorax are relieved by tapping. 

Cough, until helped by the increasing strength of the 
heart, and consequent better circulation, will often re¬ 
quire attention, codeine proving satisfactory. 

Constipation is managed in the usual ways. 

5. Diet. This should be bland and easily digestible. In 
cases with much edema it is usual to restrict the fluid in¬ 
take, as is done in chronic parenchymatous nephritis 
(q.v.). 

6. Baths. Various mineral baths, especially those of 
Bad Nauheim, in Germany, enjoy a great reputation for 
their beneficial action on cases of chronic valvular dis¬ 
ease. The baths probably help because they tend to de¬ 
plete the system of toxic products, and the entire “cure” 
aids mainly because the patient is away from home, busi¬ 
ness cares and worries, and able to devote 24 hours a day 
to the task of recovery. Nauheim baths, as far as their 
chemical composition is concerned, can be duplicated in 
the tub at home, but the results are not so good as those 
seen in the health resort. Moreover, these measures can¬ 
not be resorted to in badly decompensated cases. 


58 


CLINICAL MEDICINE FOR NURSES. 


7. Exercise. When the heart is again fairly well com¬ 
pensated, carefully graduated exercises are of great bene¬ 
fit in increasing the strength and endurance of the heart 
muscle. These exercises consist usually in various move¬ 
ments of arms, legs, and body against a certain amount 
of resistance offered by the nurse. They must be ex¬ 
plained and illustrated in detail, by the physician, and 
must be carried out with great care, as their abuse may 
lead to irreparable harm. 

8. Convalescence. This period is long and protracted. 
Details with regard to its management can hardly be given 
as each case becomes a law unto itself. Moreover, it is 
only rarely that the nurse will be called upon to remain 
after the patient has regained sufficient strength and cir¬ 
culatory endurance to be able to look after his ordinary 
wants and to move about the house. The purpose of 
this chapter has been to set forth measures and methods 
in the acute stages of heart failure with which every nurse 
must come in contact. 


CHAPTER VIII. 


MYOCARDITIS AND ANEURYSM OF THE AORTA. 

Myocarditis. 

Myocarditis, as the name indicates, is an inflammation 
of the myocardium or heart muscle itself. The disease 
may be acute or chronic. Cases of acute myocarditis 
hardly ever occur primarily, but almost always as a com¬ 
plication of an acute infectious disease such as diph¬ 
theria, typhoid fever, pneumonia, or rheumatic fever. 
Hence, acute myocarditis is almost invariably of toxic 
origin. The fibres of the heart muscle are swollen, show 
evidences of granular degeneration, and their striations 
are blurred and indistinct. 

Acute Myocarditis. 

Symptoms. There may be very few, or almost none. 
Frequently, however, there is 

1. Pallor of the face, which is striking and persistent. 

2. Vomiting. 

3. Weakness and listlessness not accounted for by the 
primary disease from which the patient may be con¬ 
valescing, the patient giving the impression of being pro¬ 
foundly ill. 

4. Rapid pulse, not particularly marked, the rate being 
usually about 100. There may or may not be irregularity 
of the pulse. 

5. Feeble and unstable pulse, a very slight exertion be¬ 
ing sufficient to send up the pulse-rate out of all propor¬ 
tion to the degree of effort. 


(59) 


60 


CLINICAL MEDICINE FOR NURSES. 


The course of the disease is variable. Death may 
occur within two or three days. The presence of the 
condition may be unrecognized, and sudden death occur, 
or alarming symptoms may alternate with periods of 
almost perfect well-being. The outlook is always grave 
if the degree of myocarditis is at all advanced. 

Treatment. There is no measure that will directly 
influence the damaged heart muscle favorably. Proper 
treatment for the pre-existing disease is, of course, an 
essential. 

As soon as signs and symptoms of myocarditis are de¬ 
tected, “the indication is to maintain the patient in abso¬ 
lute repose of mind and body. Physical effort is danger¬ 
ous, and so long as cardiac weakness exists the patient 
must remain in bed. He should receive as much highly 
nutritious and simple food as he can assimilate—milk, 
eggs, broth, etc. The bowels are to be kept active, 
though depleting purgatives are to be avoided. Strych¬ 
nine is highly serviceable. ... In conclusion, it 
may be repeated that the agencies of greatest service are: 
rest, food, strychnine, and stimulants, in the order 
named” (Babcock). 

Chronic Myocarditis. 

Etiology. 

1. Degenerative changes in the coats 

of the arteries (arterioscler¬ 
osis) 

2. Chronic nephritis, both parenchy¬ 

matous and interstitial 

3. Hard toil. 

4. Poor quality of blood. 


j by augment- 
ing resistance 
! to the heart. 


MYOCARDITIS AND ANEURYSM. 


61 


(a) Cancer. 

( b ) Chronic suppurations. 

(c) Anemia. 

(d) Chronic diarrhea. 

( e ) Insufficient food. 

5. Toxins of acute infectious diseases. 

Symptoms. These are notoriously uncertain. Often 
there are no symptoms, the heart doing its work fairly 
well until of a sudden it stops, exhausted, and the pa¬ 
tient falls dead. Heart action may be feeble and irregu¬ 
lar; there may be dyspnea, edema, and all the symptoms 
detailed under failure of compensation in the section on 
chronic endocarditis, resulting from a combination of 
failing heart muscle and dilatation of all the chambers 
of the heart. 

Osier has grouped cases of chronic myocarditis in the 
following practical manner: 

1. Those in which sudden death occurs with or with¬ 
out previous indications of heart trouble. 

2. Cases in which there are cardiac arrhythmia, short¬ 
ness of breath on exertion, attacks of asthma, collapse 
symptoms, with sweats and extremely slow pulse. 

3. Cases in which there are cardiac insufficiency and 
symptoms of dilatation of the heart. 

The outlook in cases of chronic myocarditis is very 
grave. The heart is permanently damaged, and in addi¬ 
tion there is the ever-present action of the exciting cause, 
whatever it may be, so that, while recovery from attacks 
of heart failure frequently occurs, their recurrence is to 
be expected, and eventually a fatal seizure is bound to 
come. 

Treatment. Rest is first in importance for the pa¬ 
tient—prolonged rest both of mind and body. Every ex- 


62 


CLINICAL MEDICINE FOR NURSES. 


ertion must be prevented, as the heart needs freedom 
from all possible strain in order to recuperate. Restless¬ 
ness is well acted upon by morphia. Strychnine has 
found much favor in toning up the heart. Stimulants, 
especially aromatic spirits of ammonia, are often very 
useful. The diet must be light, and the amount of fluids 
must frequently be restricted, especially in cases with 
edema. As in the case of acute myocarditis, the bowels 
must be kept well open, but the patient’s strength must not 
be sapped by the use of drastic purgatives. No set rule 
can be given for the management of these cases, as the 
frequently complicating nephritis and arteriosclerosis 
make of each case an individual problem. The nurse 
must be ever watchful for signs of returning failure on 
the part of the heart, for lack of proper elimination on 
the part of the kidneys, and in the control of the pa¬ 
tient’s daily life must err on the side of caution, for any 
excessive exertion may at once destroy all the advan¬ 
tage gained by weeks of patient and unremitting care. 

Aneurysm of the Thoracic Aorta. 

By aneurysm is meant dilatation of an artery. Aneu¬ 
rysms may occur in any artery of the body, but this 
section concerns itself solely with aneurysm of the aorta. 
Aortic aneurysms vary in size from that of a walnut to 
that of a child’s head. 

Etiology. Aneurysms originate from the gradual 
giving way of the aorta, owing to disease of the wall of 
the artery, especially of the media or middle coat. Fac¬ 
tors entering prominently into the formation of aortic 
aneurysms are: 

1. Arteriosclerosis. Almost always present. 


MYOCARDITIS AND ANEURYSM. 


63 


2. Syphilis. Now believed to be a factor in the 
causation of the vast majority of aortic aneurysms. 

3. Age. Usually occurs in individuals over 40. 

4. Sex. Males affected eight times as frequently as 
females. 

5. Alcoholism and occupations involving great physical 
exertion. 

Symptoms. These are very varied, as can readily be 
imagined when it is borne in mind that the sac, or 
tumor, growing from the aorta, may spread in any direc¬ 
tion. Most of the symptoms produced by aneurysm are 
due to pressure upon adjacent structures, such as the 
lungs, trachea, esophagus, ribs, and various nerves run¬ 
ning through the chest. Thus it will be seen that to 
describe all symptoms would necessitate an anatomical 
discussion as to the relationship of the thoracic contents, 
and mention of every direction in which an aneurysm 
could exert pressure. This would involve an amount 
of detail that is obviously beyond the scope of a short 
lecture. 

There are, however, certain general features shared 
to a greater or less extent by all aneurysms, whatever 
their position along the course of the thoracic aorta, and 
these will now be briefly considered: 

1. Pain. One of the earliest and most constant symp¬ 
toms. Its intensity depends upon the direction in which 
the sac presses. It is described as boring, grinding, cut¬ 
ting, burning, etc. It is apt to be very constant, unlike 
chest pains arising from causes other than the growth of 
a tumor. It may be aggravated or lessened by a change 
in position, according as pressure upon the intercostal 
nerves is increased or lessened. 


64 CLINICAL MEDICINE FOR NURSES. 

2. Dyspnea. Very common, but varies much in sever¬ 
ity. Most marked when the aneurysmal sac presses upon 
the trachea, large bronchi, or lungs. 

3. Cough. Common, but also very variable. May be 
slight, or at times the most distressing symptom. When 
due to pressure on the trachea, the cough has a harsh 
quality, known as “brassy.” Sometimes cough is hoarse, 
due to paralysis of a vocal cord. 

4. Expectoration. Usually associated with cough. 

5. Hemoptysis. This frequently occurs, the blood 
coming from raw areas in the bronchi, from lung destruc¬ 
tion due to pressure, or from the sac itself, in which case 
it is spoken of as ‘‘weeping aneurysm.” 

6. Dysphagia. Caused when the tumor presses upon 
the esophagus. Swallowing may be moderately or ex¬ 
tremely painful, and it may gradually become impossible 
for food to pass into the stomach. 

7. Perceptible tumor. At times the sac projects out¬ 
ward, eats its way through the ribs, and bulges from the 
front of the chest. 

Course of the Disease and Prognosis. The course is 
usually lengthy, the tumor gradually growing larger, and 
causing more and more pain and suffering through the 
constantly increasing pressure. The outlook is bad. 
Occasionally a small sac will stop growing, and a condi¬ 
tion of arrest be brought about, but the walls of the sac 
are the walls of a diseased vessel, and under the constant 
strain of pressure from the contained blood they usually 
end by giving way. Death occurs sometimes by rupture 
of the sac, with immediate profuse hemorrhage, or else 
as a result of the mechanical interference with respira¬ 
tion or circulation, from exhaustion, or from starvation, 
as when the esophagus is obliterated by pressure. 


MYOCARDITIS AND ANEURYSM. 


65 


Treatment. This is very unsatisfactory. Attention 
must be directed to the underlying cause, when discover¬ 
able, and in syphilitic patients arsphenamin and mercury 
are used extensively. 

Rest in the recumbent position is essential, if this posi¬ 
tion does not aggravate any of the symptoms. Attempts 
must be made to reduce arterial tension, and to lessen the 
volume of blood. Tufnell, of Dublin, has recommended 
a very rigid and restricted diet, with which good results 
have been obtained. His dietary consists of 2 ounces of 
bread and butter with 2 ounces of milk for both break¬ 
fast and supper, and 2 to 3 ounces of meat and 3 to 4 
ounces of milk for dinner. Few patients have the hard¬ 
iness to persist with such a diet any considerable time; 
but food restriction, and particularly fluid restriction, are 
important. 

Among drugs, iodide of potassium holds first place. 
It is usually administered in moderate doses, and fre¬ 
quently has a most beneficial effect upon pain. 

The remainder of the treatment is symptomatic, and in 
the vast majority of cases morphia will have to be freely 
resorted to before death brings relief from suffering. 
Various surgical procedures have been attempted, all of 
doubtful value. 


5 


CHAPTER IX. 

BLOOD-PRESSURE. 

By “blood-pressure” is meant the amount of pressure 
that the blood is under in the arteries. While in physio¬ 
logical experiments venous and capillary pressure are 
also determined, in the actual practice of medicine the 
arterial pressure is the only one whose determination is 
in general use. The importance of blood-pressure lies not 
in the pressure the fluid blood itself is under, but in the 
information it gives with regard to the amount of pres¬ 
sure the arterial walls have to resist, and the amount of 
resistance the heart has to overcome. A nurse will not 
be required to estimate blood-pressure, but she will see 
it done so often, and hear the results of this method of 
examination discussed so frequently, that she should 
know enough of the subject to appreciate its value and 
significance. Moreover, there are several diseases so de¬ 
pendent upon and so intimately associated with varia¬ 
tions in blood-pressure that their proper understanding 
is impossible without an appreciation of the significance 
of arterial tension. 

The instrument employed for the determination of 
blood-pressure is known as the sphygmomanometer. 
There are many varieties on the market. All possess a 
cuff, made usually of cloth or leather, lined with a rub¬ 
ber bag that can be inflated with air through a tube by 
means of a little pump. This bag is also connected by 
another tube with a column of mercury running on a 
scale graduated in millimeters, the unit of estimation of 
blood-pressure being a millimeter of mercury. Thus, if 
( 66 ) 


BLOOD-PRESSURE. 


67 


a certain pressure is said to be 160, 160 millimeters of 
mercury is meant. When the so-called “systolic” blood- 
pressure is to be determined, the cuff is attached to the 
upper arm, with the rubber bag lying next to the skin 
and covering the inner side of the arm where runs the 
brachial artery. The bag is then filled with air by means 
of the pump until enough constriction is exerted to ob¬ 
literate the pulse at the wrist. During this procedure the 
column of mercury rises rapidly, due to the pressure ex¬ 
erted upon it from the air within the bag. When the 
radial pulse can no longer be felt, a small thumb-valve in 
the pump is slightly opened, letting any desired amount 
of air escape from the bag. Air is gradually allowed 
to escape until the radial pulse can again be felt because 
of the lessening of compression over the brachial artery. 
The reading on the scale of the mercury column at the 
time the first faint beat can be felt at the wrist constitutes 
the systolic pressure. 

Latterly there has come into use the “auscultatory” 
method of blood-pressure estimation, by which means 
both systolic and diastolic pressure (to be mentioned 
presently) are determined. This method will not be 
described, as it is rather complicated, and would be of no 
practical use to the nurse. 

There are five factors which go to maintain normal 
blood-pressure: 

1. The energy of the heart. 

2. The resistance offered to the heart by the passage 
of the blood through the arteries. 

3. Vasomotor tone. 

4. Volume of blood. 

5. Viscosity of blood. When blood is watery, pressure 
is invariably low. 


68 


CLINICAL MEDICINE FOR NURSES. 


Most of these factors are self-evident, but No. 3 
(vasomotor tone) requires a word of explanation. By 
vasomotor tone is meant the average general tonus or 
steadily maintained pressure of the arterial walls upon 
the blood running within them. This tonus may, and 
does, vary greatly in normal persons at different times 
and in different parts of the body, depending upon the 
particular needs of the particular organ or tissue at any 
particular time. The mechanism of vasomotor tone is 
reflex in origin, and is governed by the sympathetic nerv¬ 
ous system. Sympathetic nerve-fibres run in the arterial 
walls, some being called vasoconstrictors, i.e., causing the 
muscle fibres in the walls of arteries to contract, and thus 
to narrow the calibre of the vessel; others known as vaso¬ 
dilators, causing the muscle-fibres in the walls of the 
arteries to dilate, and thus to unden the calibre of the 
vessel. Thus, during digestion, due to vasodilator 
action, the blood-vessels of the intestinal walls dilate, and 
more blood is brought to the parts. Again, during the 
active exercise of any muscle or group of muscles the 
vessels within the muscles dilate in order that more blood 
may be supplied. Application of cold, on the other 
hand, causes vasoconstriction and a blanching or pallor 
of the skin. Vasomotor tonus and vasomotor action 
are the great equalizers of blood-pressure all over 
the body, and one of the most important factors in main¬ 
taining an even circulation throughout the body, the 
various portions of which are subjected to such diverse 
and unexpected demands. 

Blood-pressure is divided into two chief phases: 

1. Systolic Pressure. This term is applied to the 
blood-pressure within a given artery, when the greatest 
force is exerted within it, i.e., during ventricular systole. 


BLOOD-PRESSURE. 


69 


2. Diastolic Pressure. This is the degree of pressure 
exerted within an artery during cardiac diastole, and 
represents the lowest pressure occurring in the vessel. 

The so-called pulse-pressure is obtained by subtracting 
the diastolic pressure from the systolic pressure, and 
denotes the total variation in pressure occurring during 
a cardiac cycle, thus: 

Systolic pressure . 145 mm. of mercury. 

Diastolic pressure. 100 “ “ 

Pulse pressure. 45 

Blood-pressure is influenced normally by a variety of 
factors, some of which are here briefly mentioned: 

(a) Age. Low in childhood, gradually rising with 
advancing years. 

( b ) Sex. Slightly lower in women than in men. 

(c) Digestion. Higher during its greatest activity. 

( d ) Muscular development. Higher in those well 
developed. 

( e ) Mental worry or fatigue. Lowered. 

(/) Altitude. Slightly lowered. 

Normal Blood-pressure. Janeway, in more than 2000 
blood-pressure determinations, has found the high nor¬ 
mal limit of systolic pressure, with very few exceptions, 
to be 145 mm.; his figures for women are 10 mm. less. 
The same authority believes normal diastolic pressure 
to be from 25 to 40 mm. below the systolic pressure. 

As a general guide for the estimation of normal sys¬ 
tolic pressure, Faught has formulated the following rule: 
“Consider the normal average systolic pressure at the age 
of 20 to be 120 mm. of mercury; then for each year of 
life above this add y 2 mm. to 120.” Thus, for a man of 
50 the rule would read: 120 + 15 (y 2 of 30) = 135 mm. 
of mercury as normal systolic pressure. 





70 


CLINICAL MEDICINE FOR NURSES. 


Abnormal Blood-pressure. Abnormal blood-pressure 
can be classified under two heads: 

1. Hypotension—lowered blood-pressure. 

2. Hypertension—heightened blood-pressure. 

1. Hypotension occurs in connection with the follow¬ 
ing conditions: 


Approaching death. 

Mitral stenosis. 

Paroxysmal tachycardia. 

Shock and collapse. 

Hemorrhage, external or internal. 

Infections, especially— 

I. Tuberculosis. 

II. Typhoid or any continued fever. 

III. Cholera or any severe diarrhea. 

Any wasting condition— 

I. Cancer. 

II. Pernicious or severe secondary anaemia. 
Diabetes. 

Neurasthenia. 

Effects and Danger of Hypotension. “The direct effect 
of a falling blood-pressure is the accumulation of an ab¬ 
normal amount of blood in the veins, and a slowing of the 
current in the arteries. This will affect the capillary cir¬ 
culation, and interfere with the nutritive and secretory 
processes which depend upon it. The most serious effect 
is on the heart, as it has been shown that complete loss 
of vasomotor tone soon leads to death, because of the 
gradual accumulation of nearly all the blood in the body 
on the venous side, so that the heart has no blood upon 
which to act” (Faught). 

2. Hypertension. This condition is an accompaniment 
of two of the most frequent chronic diseases of middle 


O) 

(b) 

(0 

(d) 

(0 

(/) 


(sO 


(*) 

(0 


BLOOD-PRESSURE. 


71 


and old age—arteriosclerosis and chronic interstitial 
nephritis. 

A condition of hypertension exists when the systolic 
pressure is over 160 mm. of mercury. When the systolic 
reading reaches 200 mm. the condition is serious, and 
when over 200 mm. it becomes dangerous, though many 
individuals are met with that enjoy relatively good health 
together with an alarmingly high blood-pressure. There 
are many combinations of and relationships between the 
systolic and diastolic pressures, which will not be dis¬ 
cussed here, as they belong to the province of the physi¬ 
cian rather than to that of the nurse. 

Hypertension is usually, though by no means always, 
present in connection with the following conditions: 

. (a) Arteriosclerosis. 

( b ) Chronic interstitial nephritis. 

(c) Cardiovascular-renal disease. 

( d ) Apoplexy. 

( e ) Acute nephritis. 

(/) Chronic parenchymatous nephritis. 

(g) Uremia. 

The management of both abnormally low and abnor¬ 
mally high blood-pressure will not be entered into here, 
as it is dealt with in connection with the diseases in which 
those conditions occur. 


CHAPTER X. 

THE URINE. 

The urine is both an excretion and a secretion. It is 
an excretion in the sense that its component parts are 
no longer of any use to the body and hence must be 
eliminated, and it is a secretion in the sense that it is 
the product of the activity of a gland, the kidney. 

Normal Urine. Always aqueous. Usually transpar¬ 
ent, though it may be clouded by— 

Mucus, earthy phosphates of calcium and magnesium, 
or by urates, these last usually giving a “brick-dust” 
sediment. 

Color. Pale lemon-yellow to reddish-brown. 

Reaction. Usually acid, due to the presence of acid 
phosphates of sodium and calcium. The acidity of the 
urine varies at different times. In the early morning it 
is highest. After meals, i.e., during the period of great¬ 
est digestive activity, urinary acidity is lowest. If food 
is mainly vegetable and rich in alkaline salts, the urine 
may become neutral or even alkaline. 

Specific Gravity. Varies from 1.012 to 1.024. The 
early morning urine shows the highest specific gravity. 

Amount in Twenty-four Hours. Roughly speaking, 
1500 c.c.—3 pints or 50 ounces. 

The amount of urine is affected by several factors— 

1. Intake of fluids. The amount of urine is increased 
proportionately to the amount of liquid drunk, and dis- 
(72) 


THE URINE. 


73 


proportionately when some of the fluids taken have a 
markedly diuretic action, e.g., beer, coffee. 

2. Intake of food. If a large amount of solid food is 
taken, together with a relatively small amount of liquid, 
the urine will be decreased in amount. 

3. Digestion. The amount of urine is at its greatest 
a few hours after a meal, and at its lowest during the 
early morning hours. 

4. External temperature: 

1. Cold. Amount of urine greatly increased, and 

specific gravity lowered, because the skin, 
which is the other great channel for the elimi¬ 
nation of fluids, is not active. We do not per¬ 
spire freely in winter. 

2. Heat. Amount of urine decreased, and specific 

gravity raised, because of increased fluid elimi¬ 
nation through the skin. 

5. Exercise. Increases amount of urine because of 
increased metabolism going on throughout the body. 

6. Drugs. Some increase urinary flow; others de¬ 
crease it. 

Composition of Normal Urine. In a twenty-four-hour 
specimen totalling 1500 c.c. there will occur about 72 
grams of solids. 

These solids and their approximate proportions in 
grams are as follows: 

Gms. 


Uric acid (urates) .* • • • 

Hippuric acid... 0-40 

Creatinin, xanthin .'I 

Hypoxanthin, guanin . }■ 1121 

Ammonium salts .J 








74 CLINICAL MEDICINE FOR NURSES. 

Inorganic salts: 

Sulphates, phosphates and chlorides of sodium") 


and potassium . j Gms. 

Phosphates of calcium and magnesium.J* 27.00 

Organic salts: 

Acetates ...j 

Sugar. Trace. 


Gases. N and CO 2 . 

(This table is given merely to show what an exceed¬ 
ingly complex substance urine is). 

A few words should be said about urea. This is the 
most abundant organic constituent of urine. Interest in 
this substance centers in the fact that it is the chief end- 
product of proteid metabolism. Proteid is the substance 
that is most difficult of elimination for the kidneys. 
Therefore estimation of the amount of urea eliminated 
can indicate to quite an accurate degree the state of kid¬ 
ney efficiency. Of course, in order to properly estimate 
the urea output, the exact amount of proteid intake must 
be accurately known, otherwise the urea estimation is 
obviously quite useless. 

The estimation of uric acid and of creatinin are fre¬ 
quently made nowadays, not because of the intrinsic im¬ 
portance of these substance, but because, like urea, they 
indicate the amount of proteid elimination on the part of 
the kidney. 

Abnormal Urine: 

Color. Pale in diabetes. 

Pale in hysteria. 

Pale in chronic interstitial nephritis. 

Deep brown or almost red in practically all 
acute fevers and in acute nephritis. 

Dark in liver disease and jaundice, due to 
bile pigment. 

Brown to bright red when containing blood. 





THE URINE. 


7 5 


Changed by drugs: 

Blue after taking methylene blue. 

Brown-smoky after taking carbolic acid. 

Bright yellow after taking santonin. 

Amount in Twenty-four Hours. Usually considered 
pathological when under 500 c.c. (1 pint) or over 3000 
c.c. (3 quarts). 

Small output of urine is known as oliguria. Oliguria 
occurs in— 

1. Cardiac disease, with low blood-pressure. 

2. Acute fevers. 

3. Acute nephritis and chronic nephritis with edema. 

4. Cholera and all severe diarrheas. 

5. Eclampsia with uremia. 

(Obstructions of a mechanical nature, tumors, etc., 
are not here considered.) 

Large output of urine is known as. polyuria. Polyuria 
occurs in— 

1. Diabetes mellitus. 

2. Diabetes insipidus. 

3. During absorption of large effusions : 

(a) Pleural. 

(b) Peritoneal. 

4. Convalescence from typhoid fever and from other 
acute infections. 

5. Chronic nephritis without edema. 

6. Exophthalmic goitre (Graves’s disease). 

Albuminuria, i.e., albumin in the urine. The presence 

of albumin in the urine is almost always a pathological 
finding, though its mere presence by no means signifies 
kidney disease. 

Albumin in the urine may be due to the presence of 


76 


CLINICAL MEDICINE FOR NURSES. 


pus from a cystitis, or to the presence of blood from a 
hemorrhage somewhere in the urinary tract. 

Albuminuria may be— 

1. Cyclic. Appearing, disappearing, and reappearing 
at certain definite intervals. Usually of no known sig¬ 
nificance. 

2. Dietetic. Appearing after a meal over-rich in 
proteid. 

3. Febrile. Due to degenerative changes in the kidney 
taking place during the height of the acute fevers. These 
changes are usually transitory and complete recovery is 
the rule. 

4. Toxic. Poisoning by any substance, especially 
ether. 

5. Renal, i.e., the result of a true nephritis, acute or 
chronic. 

Glycosuria, i.e., sugar in the urine. Sugar in the 
urine is a far rarer condition than is the presence of 
albumin. Sugar may appear in a transitory manner after 
meals rich in sugar, but persistent glycosuria is always 
pathological. In the large majority of cases the cause 
of persistent glycosuria is diabetes mellitus. 

Indicanuria, i.e., excessive amount of indican in the 
urine. This condition occurs when an undue amount 
of toxic material is being absorbed into the body from the 
intestinal tract. 

Pyuria, i.e., pus in the urine, may occur as the, result 
of a urethritis, a cystitis, or as a result of a kidney abscess, 
a pyelonephritis, or tuberculosis of the kidney. 

Some Suggestions for the Collection of Urinary 
Specimens. When taking charge of a case it is well 


THE URINE. 


77 


for the nurse to have a specimen of urine ready for the 
physician at his visit on the following day, even if a re¬ 
quest for it has not been made. Urinary specimens may 
be divided into three classes: 

1. Specimen of mixed urine. 

2. Specimen of twenty-four-hour urine. 

3. Catheterized specimen for special examinations. 

Classes 2 and 3 will be specially requested by the 

physician. Where “a specimen of urine” is asked for, 
the nurse can take it for granted that “mixed” urine is 
meant— i.e. y some passed in the evening mixed with some 
passed in the morning. Save when specially requested, 
or when the output of urine is exceedingly scanty, a 
specimen should not consist entirely of urine passed at 
one voiding. If a twenty-four-hour specimen is re¬ 
quested, the nurse should always ask the physician if he 
wishes the entire quantity, or whether a portion of the 
total urine will suffice; and the number of ounces passed 
in the twenty-four hours should always be plainly re¬ 
corded on the label accompanying the specimen. 

A four-ounce bottle should be used for the specimen of 
urine, and, unless impossible to do so, the bottle should 
be entirely filled. There are few things more irritating 
to the physician than to have specimens of urine totalling 
from half an ounce to an ounce and a half received from 
patients passing fifty times that amount in twenty-four 
hours; and yet these “homeopathic” specimens are con¬ 
stantly being sent to the laboratory. If there is plenty of 
urine, let the specimen be generous. The bottle should, 
of course, be clean—not necessarily sterile, unless the 
physician particularly requests this. It should be firmly 
stoppered with a well-fitting cork. Fruit jars, sal 
hepatica jars, Pluto water bottles with their little tin 


78 


CLINICAL MEDICINE FOR NURSES. 


caps for corks, are all unsuitable for urinary speci¬ 
mens. The nurse must be certain that the previous con¬ 
tents of the bottle have all been done away with, as in 
the author’s experience one case is recalled where a 
marked sugar reaction was obtained, which was subse¬ 
quently traced to the specimen bottle having contained 
some substance rich in glucose. 

The name of the patient, the date, the total amount of 
urine if the specimen is a “twenty-four-hour specimen,” 
and the hours of voiding, if the specimen is “mixed,” 
should all be plainly written on a label, which should be 
pasted on the bottle. It may seem superfluous to men¬ 
tion all these details, but their enumeration is the result 
of several years’ experience in the laboratory with all 
manner of specimens, containers, legible labels, illegible 
labels, and, last of all, no labels! 

The nurse should be sure to deliver or send all speci¬ 
mens promptly to the physician’s laboratory. If she 
thinks there may be some delay, she should ask the 
physician what to add to the urine as a preservative. A 
small piece of thymol or a few cubic centimeters of 
chloroform are commonly used. Urine rapidly decom¬ 
poses, and “stale” urine is unfit for examination. 

Urinary Examination. It is not within the province 
of the nurse to examine urinary specimens. There are, 
however, four tests in connection with urinary analysis 
that any nurse should be able to perform satisfactorily, 
and these tests are so common that she should be 
familiar with them: 

1. Determination of the reaction of the urine. 

2. Determination of the specific gravity of the urine. 

3. Determination of the presence or absence of 

albumin. 


THE URINE. 


79 


4. Determination of the presence or absence of 
sugar. 

1. Determination of the Reaction of the Urine. Dip 
a piece of blue litmus paper in the urine. If it turns red, 
the urine is acid. If it does not change color, dip a piece 
of red litmus paper in the urine. If it turns blue the 
urine is alkaline. If neither paper changes color, the urine 
is neutral. 

2. Determination of the Specific Gravity of the Urine. 
Pour urine into a cylindrical jar made for the purpose, 
or into a 100-c.c. graduate. Fill the jar or graduate to 
within an inch of the top. See that no bubbles have 
formed on the surface of the urine. Drop the urinometer 
or specific gravity float into the urine with a spinning 
motion. Allow it to settle and read the specific gravity 
on the scale of the urinometer, reading at the bottom of 
the meniscus. The meniscus is that portion of the fluid 
that appears to be “climbing up” the sides of the gradu¬ 
ate. This takes place because of capillary attraction. 
The reading of the urinometer scale should be made at 
the level of the fluid, which is appreciably below the top 
of the meniscus. 

3. Determination of the Presence or Absence of Al¬ 
bumin. ( a ) Fill a small test-tube two-thirds full of 
urine. Hold it at its lower end, and boil the upper inch 
of urine in the Bunsen burner or alcohol flame. If no 
cloud appears in the urine, albumin is absent. If a cloud 
appears, add two or three drops of 3 per cent, acetic 
acid. If the cloud disappears it is due to phosphates. If 
it persists and grows more dense on boiling again, albu¬ 
min is present. 

All variations may exist in the amount of cloud ob¬ 
tained, depending upon the amount of albumin. The 


80 CLINICAL MEDICINE FOR NURSES. 

faintest film may be seen, or the urine may boil almost 
solid. 

( b ) Pour about 2 c.c. of cold nitric acid (HNO 3 ) 
into a small test-tube. With the aid of a dropper allow 
about 1 c.c. of urine to flow slowly down the side of the 
test-tube and to overlay the nitric acid. In the presence 
of albumin a white ring is seen at the point of contact 
of nitric acid and urine. 

4. Determination of the Presence or Absence of Sugar. 
1. Fehling’s solution is used for this test. It consists of 
two elements : 

I. A solution of copper sulphate. 

II. A solution of rochelle salts. 

To perform the test: In a small test-tube place 1 c.c. 
of solution I. Add 1 c.c. of water. Then add 1 c.c. of 
solution II, and 1 c.c. of water. Bring to a boil. Add 1 
c.c. of urine and boil again. If the solution remains a 
clear beautiful blue, sugar is absent. If it turns to a 
dirty green, or to a reddish-yellow, or to an actual red, 
sugar is present. 

2. Benedict’s test. 

In the 1923 edition of his book on diabetes, Dr. E. P. 
Joslin, than whom there is no greater authority, gives the 
following as the most accurate method of performing this 
test which he considers more accurate than Fehling’s. 
“Seven cubic centimeters (an ordinary teaspoon holds 
about 5 c.c.) of Benedict’s solution are placed in a test- 
tube. Eight (not more) drops of the urine to be exam¬ 
ined are added, the tube is agitated to mix the urine and 
solution and then placed in water that is already boiling. 
After being in the boiling water for five minutes, the tube 
is removed and examined for evidence of reduction. In 
the presence of glucose the entire body of the solution 


THE URINE. 


81 


will be filled with a precipitate, which may be greenish 
yellow or red in tinge, according to whether the amount 
of sugar is slight or considerable. As used with urine the 
test is sufficiently delicate to detect quantities as small as 
0.08 or 0.1 per cent, sugar.” 

Further urinary tests will not be mentioned here, as 
it is felt that they lie outside the sphere of the trained 
nurse, unless she wishes to become a laboratory technician. 


6 


CHAPTER XI. 

UREMIA. 

Uremia is not a disease in itself, but a condition that 
occurs both alone and as a complication of many dis¬ 
eases. Thus, we often say that such-and-such a patient 
is doing badly—“he is becoming uremic”—meaning 
thereby that the condition recognized as uremia is set¬ 
ting in. 

The cause of uremia remains as yet unknown. There 
are many theories advanced, but none has hitherto met all 
requirements. It is definitely known that uremia is of 
toxic origin, and arises from failure on the part of the 
body to properly eliminate its waste-products. It has 
been claimed by some that uremic patients are those 
whose urine has lost its toxicity. Urine should be toxic 
because of the waste-products it contains; when it loses 
its toxicity, the waste-products are not excreted, and 
hence are stored up in the body. 

Acute Uremia. A typical attack of acute uremia 
may appear without any previous signs of illness, or 
else the condition may appear as the terminal factor in 
many diseases, especially chronic nephritis without edema. 

James B. Herrick gives the following description of an 
uremic attack which cannot be improved upon: “When 
a convulsion occurs there is seldom any aura, as in epi¬ 
lepsy, nor is there the cry so often heard in that disease. 
The eyes roll upward and usually to one side, the pupils 
dilate, and for a moment the patient seems gazing with a 
fixed stare into distance. Then a jerking of the angles 
of the mouth is seen, the head draws to one side, the 

( 82 ) 


UREMIA. 


83 


muscles of the face and neck become clonically convulsed, 
the fingers and arms are flexed and likewise convulsed, 
and soon the entire musculation of the body is in irregular, 
jerky, violent motion. The face becomes livid or purple, 
foaming saliva issues from the mouth, and it may be 
streaked with blood that comes from a bitten tongue, the 
(pulse grows rapid and weak, perhaps irregular. During 
the seizures there may be involuntary evacuation of urine 
and feces. A few seconds or minutes are consumed by 
the attack, which ends with a quieting of the muscular 
spasm, a deep-drawn inspiration, and a rather prompt re¬ 
covery of consciousness. If, however, the patient has 
been in a stupor or coma preceding the convulsion, or if 
the attacks are frequently repeated, sleep, stupor, or deep 
coma will follow. Usually the patient is somewhat dazed 
for a time, and knows little more of the attack than that 
‘something has happened.’ When attacks are repeated 
at short intervals the temperature often rises, and pre¬ 
agonal temperatures of 105° or over are not unusual. 
The pulse, after frequently repeated convulsions, becomes 
rapid and weak.” 

During the attack of acute uremia there is usually 
complete or partial suppression of urine; and during the 
entire duration of uremia, whether acute or chronic, the 
amount of waste-products excreted by the kidneys is be¬ 
low par, even though the total amount of urine may be 
well up to normal. 

After the convulsive seizure blindness may occur, 
which may persist for several days. At times coma may 
develop without any convulsion occurring. Nausea and 
vomiting may be prominent symptoms. 

Chronic Uremia. By chronic uremia is meant that 
group of symptoms which denote insufficient elimination. 


84 


CLINICAL MEDICINE FOR NURSES. 


These symptoms may persist for a long or short time, 
may clear up entirely under treatment, or at any moment 
the patient may be thrown into an attack of acute uremia. 
Chronic uremia hardly ever appears at the first sign of 
ill health; it is almost always a complication of some 
pre-existing ailment, most frequently of chronic nephritis. 
It is important for the nurse to be familiar with some 
of the manifestations of chronic uremia, as thus she can 
observe changes in the patient, and, what is more, can 
appreciate their significance. 

The symptoms to which chronic uremia gives rise will 
be mentioned under the headings of the various systems 
of the body: 

1. Cutaneous. Itching. May be only slight or else 
universal and intense. There may be many varieties of 
skin eruptions. 

2. Respiratory. Dyspnea, which may be 

(a) Continuous. 

( b ) Paroxysmal. 

( c ) Cheyne-Stokes. A period of moderate breath¬ 

ing followed by a period of gradually increas¬ 
ing deep breathing, which in turn gradually 
fades away, and is followed by a period of 
very shallow breathing. 

3. Circulatory. 

(a) High arterial tension. Very commonly occurs, 

but its absence is by no means invariably a, 
favorable sign. 

( b ) Heart failure. Usually myocardial degenera¬ 

tion (see chapter on Myocarditis). Common. 
Many deaths from: this cause. 


UREMIA. 


85 


(c) Rather slow pulse. May be some irregularity. 
(During convulsive seizures of acute uremia 
pulse may be small, soft and rapid.) 

4. Nervous. 

(a) Convulsions. These have been described. In 

chronic uremia there may be merely muscular 
twitchings which never reach the dignity of 
a convulsion. 

( b ) Dimness of vision. A sense of a film before 

the eyes. An important symptom of advanc¬ 
ing chronic uremia. 

(c) Gradually increasing mental dullness, eventually 

passing into semi-consciousness and coma. 

(d) Headache and giddiness. Very frequent and 

very important. Their increase is a bad sign, 
and their lessening a good sign. 

5 . Gastro-intestinal. 

(a) Loss of appetite. 

(b) Nausea and vomiting. May be the first symp¬ 

tom that attracts attention. May be slight 
or very intense. 

(c) Hiccough. Violent and persistent. A very bad 

sign. 

( d ) Constipation. 

( e ) Diarrhea. Usually occurs only in last stages. 

Prognosis. The outlook in uremia is always grave. 
Much depends upon the condition existing before uremia 
developed. Acute uremia developing in the presence of 
an acute nephritis offers a better chance for recovery than 
acute uremia developing on top of a chronic nephritis 
with or without edema. Chronic uremia is always serious, 
and, as in the case of acute uremia, the outlook depends 


86 


CLINICAL MEDICINE FOR NURSES. 


largely upon the pre-existing condition. Usually, com¬ 
plete recovery from chronic uremia is not possible, but 
often considerable improvement can be obtained and main¬ 
tained for long periods of time. 

Treatment. “The correct treatment of nephritis is 
the best way of escaping acute or chronic uremia.” 

With the exception of the management, of the con¬ 
vulsion, for which chloroform is often necessary, the 
treatment of acute uremia is identical with that of acute 
nephritis, and therefore will be dealt with in connection 
with that disease. 

The treatment of chronic uremia is identical with that 
of chronic nephritis with or without edema, and will be 
dealt with under those headings. 


CHAPTER XII. 

NEPHRITIS (BRIGHT’S DISEASE). 

Nephritis signifies inflammation of the kidney. It 
does not include the surgical conditions of that organ, 
such as tuberculosis, kidney stone, kidney abscess, etc. 

There are many classifications of nephritis. Christian, 
of Boston, has given the one I consider most satisfactory, 
which is here reproduced. 

1. Acute nephritis. 

Subacute nephritis. 

2. Chronic nephritis. 

( a ) With edema. 

( b ) With hypertension. 

(c) Mixed or intermediate type. 

3. Essential vascular hypertension progressing into 
chronic nephritis. 

4. Renal arteriosclerosis progressing into arterio¬ 
sclerosis. 

For nurses, however, this classification is too elaborate 
and therefore will be modified as follows: 

1 Acute nephritis. 

2. Chronic nephritis. 

(a) With edema. 

( b ) Without edema. 

With or without hypertension. 

Acute Nephritis. 

(acute bright’s disease.) 

Acute nephritis is a diffuse inflammation of the kid¬ 
neys, involving practically every portion of the kidney 
structure, and brought on by a variety of agencies. 

(87) 


88 


CLINICAL MEDICINE FOR NURSES. 


Etiology. 

1. Infectious diseases, especially: 

(a) Scarlet fever. By far the most important. The 

toxin of scarlet fever seems to be particularly 
injurious to the kidneys. 

( b ) Diphtheria. 

(c) Tonsillitis. 

( d ) Various strains of streptococci.. 

Acute nephritis may occur as a complication of any 
infectious disease. 

2. Toxic agents: 

(a) Drugs, especially cantharides, turpentine, phe¬ 

nol, salicylic acid, mineral acids, alcohol, 
chloroform, mercury. 

(b) Extensive burns. Acute nephritis occurs in 

these cases as a result of toxic material 
formed from the destruction of the skin. 

(c) X-ray. 

( d ) Acute gastro-intestinal disorders. 

( e ) Disorders of metabolism. 

Diabetes. 

Gout. 

3. Cold, especially when combined with getting wet. 

4. Pregnancy, because of added strain on kidneys, 
through having to excrete for two individuals. 

Pathology. I'he kidneys are usually enlarged, and 
may be slightly edematous. The capsule peels off with 
ease. The surface is pale, and minute hemorrhages may 
be visible. 

Microscopically, the convoluted tubules are most af¬ 
fected. The lining cells are swollen, cloudy, or granular, 
and their nuclei stain badly or not at all. 


NEPHRITIS. 


89 


In the lumen of the tubules may be seen hyaline or 
granular casts, droplets of fat, red blood-cells and some 
leukocytes. The glomeruli are also affected. The cells 
lining Bowman’s capsule are degenerated and there may 
be hemorrhages into the capsule. 

Symptoms. Acute nephritis usually comes on fairly 
suddenly. At times there may be an initial chill, with 
some fever (rarely over 102°), headache, drowsiness, 



Fig. 4—Acute diffuse nephritis. (From a “Handbook of 
Pathological Anatomy and Histology,” by Delafield and Prud- 
den. Courtesy of Wm. Wood & Co., publishers.) 

nausea and vomiting. General malaise is very character¬ 
istic as is also pain in the loins. The characteristic fea¬ 
tures of acute nephritis, however, can be grouped under 
three headings: 

(1) Edema. 

(2) Urinary changes. 

(3) Uremic manifestations. 

1. Edema. The edema of acute nephritis is different 
from any other edema. It usually comes on rapidly, the 
patient having a rather pasty and puffy appearance. The 


90 


CLINICAL MEDICINE FOR NURSES. 


edema is often almost universal, not very marked at first, 
decidedly firm and pitting but little on pressure. After 
having persisted for a time it is, of course, more notice¬ 
able in the dependent portions of the body. It may be 
slight or may assume enormous proportions. 

2. Urinary Changes. The urine is always scanty (4 to 
10 ounces in twenty-four hours), or there may be com¬ 
plete suppression of urine. This latter condition can 
exist for two or three days and recovery still be possible; 
but persistent anuria is always a most serious sign. When 
urine is obtainable it is turbid, smoky, and of a reddish- 
brown color. Its reaction is acid, the specific gravity 
very high, from 1.025 to 1.035 (though in exceptional 
cases it may be as low as 1.018), and albumin is present 
usually in large amounts, though not infrequently a trace 
only is to be found. Microscopically there is seen much 
epithelium and many red blood-cells. Casts of all varie¬ 
ties—blood, epithelial, granular, and hyaline—are present 
in varying abundance. In the course of the disease there 
may be periods in which so-called “showers” of casts oc¬ 
cur, alternating with periods in which they are relatively 
scanty. One of the best signs of improvement in a pa¬ 
tient with acute nephritis is an increase in the output of 
urine, and until this occurs no case can be looked upon as 
doing satisfactorily. 

3. Uremic Manifestations. Some of these, such as 
headache, drowsiness, nausea, and vomiting, have already 
been referred to in connection with the onset of acute 
nephritis. At any time convulsions may occur, to be fol¬ 
lowed, in the most severe cases, by coma. The con¬ 
vulsions are similar in every respect to uremic convulsions. 
The pulse may be fast or slow, and is usually of high 
tension. 


NEPHRITIS. 


91 


Course of Disease. As a rule, if the patient is not 
overcome by the initial shock of the attack, improvement 
begins in two or three days, first shown, as stated above, 
by an increase in the output of urine. With this increase 
there is also a corresponding decrease in the amount of 
edema, and a lessening of the uremic manifestations. 
Acute nephritis is usually a brief disease. If it maintains 
its greatest intensity, death must come within a few days; 
if it lessens in severity, the picture becomes one of chronic 
nephritis with edema, to be presently discussed. 

Prognosis. This, as a rule, is good as far as im¬ 
mediate results are concerned. Few adults die directly 
as a result of acute nephritis. Even if the condition per¬ 
sists for some time complete recovery can take place. The 
severity of the acute attack is no indication of the likeli¬ 
hood of a subsequent chronic nephritis. It must be re¬ 
membered that uremic symptoms in a case of acute neph¬ 
ritis have by no means the same bad prognostic weight 
that they have in chronic nephritis. 

There are three possibilities confronting the patient 
with acute nephritis: 

1. Death usually due to 

(a) Uremia. 

( b ) Persistent anuria. 

(c) Inflammation of the respiratory tract. 

2. Recovery, which occurs in a large percentage of 
cases, especially when the intensity of the acute stage is of 
short duration, so that no portion of the kidney structure 
is permanently damaged. 

3. Chronic nephritis, which is the fate of many patients 
who are able to rally from the acute stage, but whose 
kidneys have suffered permanent and incurable structural 
changes. 


92 


CLINICAL MEDICINE FOR NURSES. 


The outlook in acute nephritis depends, of course, upon 
the exciting cause and upon the general condition of the 
patient before and during the disease; but it also hinges 
largely upon two factors: 

1. The amount of urine secreted by the diseased 
kidneys. 

2. The readiness with which the other avenues of 
elimination— i.e., the skin and the bowels—can be made 
temporarily to take the place of the failing kidneys. 

Treatment. Under this heading will be considered 
merely the treatment of the attack of acute nephritis— 
the after-treatment, diet, etc., being taken up under 
chronic parenchymatous nephritis. 

We have no drugs or other means at our command by 
which to cure acute nephritis. Since we cannot treat 
the disease, we must limit our efforts to treating the 
patient who has the disease. 

The objects of treatment are two-fold: 

1. To stimulate the kidneys to resume the secretion of 
urine. 

2. To secure elimination of poisons by the other chan¬ 
nels of excretion. As we cannot increase elimination 
from the lungs, treatment is directed towards: 

(a) The skin, (b) The bowels. 

General Management. The patient should be in bed, 
in a well-ventilated room, protected from draughts, and 
at a temperature not below 70°, so that the skin will not 
be dried and its pores contracted by chilliness. 

As a general rule, it is wise not to try to give any food 
for the first twenty-four hours. The patient is usually 
nauseated, and, in addition, not one iota of additional 
strain must be thrown upon the kidneys. Water, also, 
should be given in moderation. If forced upon the pa- 


NEPHRITIS. 


93 


tient, it throws an added strain upon the kidneys. Acute 
nephritis, in its intense stage, is not a condition in which 
the kidneys need “flushing out.” The thirst of the pa¬ 
tient is a good guide as to the amount of water to be 
given. It is well to give water in small amounts, and 
rather frequently. 

Christian, of Boston, believes in giving fluids very lib¬ 
erally in acute nephritis and gives the three following 
reasons in favor of its administration. 

1. Fluid intake is needed to offset fluid loss by catharsis. 

2. If fluid causes diuresis, renal elimination of toxic 
substances is favored. 

3. If fluid does not cause diuresis and even if its pres¬ 
ence tends to the production of edema, it dilutes toxins 
and later, when the crisis is over, edema so produced will 
disappear. 

When food in any form is considered advisable, milk is 
probably the best; cream can be added to it. Cereals are 
permissible, and fruits in moderation are not injurious. 
During the acute stage of nephritis it is far safer to under¬ 
feed than to overfeed. What foods are given should con¬ 
sist almost entirely of fats and carbohydrates, in order to 
call upon the kidneys as little as possible for the elimina¬ 
tion of proteins. 

Stimulation of the Kidneys to Secretion of Urine. 
Diuretics are here indicated. At first the stomach will 
hardly tolerate any drugs, but as soon as possible the 
physician in charge will order that diuretic in which he 
has the greatest faith. Lemonade is of service, a dram 
of cream of tartar being added to every pint of lemonade 
to increase the diuretic effect. The citrate and acetate of 
potassium and theobromin sodium salicylate (diuretin) 
are some of the preparations most in use. 


94 


CLINICAL MEDICINE FOR NURSES. 


Stimulation of the Other Avenues of Elimination. 
This is brought about by: 

(1) Catharsis—purgation. 

(2) Diaphoresis—sweating. 

1. Catharsis. It must be borne in mind that when 
catharsis is employed in as serious a condition as acute 
nephritis the object is not only to empty the bowels, but 
far more to abstract fluid from the body in order to 
lessen edema and eliminate poisons. To obtain this 
efifect, many copious watery stools must be obtained. 
The drugs mainly relied upon are the salines, especially 
magnesium sulphate, which is frequently given in dram 
doses of a saturated solution every half-hour until eight 
or ten free, watery movements are obtained. Many pre¬ 
fer this method to the giving of one very large dose, as 
the stomach will often not tolerate the single dose. If 
needful, the more drastic purgatives, such as elaterium 
and croton oil, may be given. 

2. Diaphoresis. Here, too, it must be emphasized that 
what is desired is not a gentle perspiration, but a pro¬ 
fuse, dripping sweat. There are several methods of ob¬ 
taining this: 

(1) Hot baths—hardly sufficient. 

(2) Wet hot pack. 

(3) Dry hot pack. 

(4) Pilocarpine hypodermically. 

The wet and dry hot packs are the means mainly re¬ 
lied upon to obtain the desired effect. The packs are given 
from two to four times daily for from twenty minutes 
to an hour each, depending upon the patient’s condition. 
During the pack an ice-cap should be applied to the head. 
The drenching sweat abstracts a large amount of fluid 
from the body, and is of great benefit. Pilocarpine is 


NEPHRITIS. 


95 


rarely used as the sole sweating agent, as once the sweat 
is started by the drug in full dosage it cannot be con¬ 
trolled, and may prove too exhausting. A small dose of 
pilocarpine is frequently given to the patient when in the 
hot pack, in order to start the sweat. 

The pain over the kidneys in acute nephritis is often 
aided by the application of the hot-water bottle or a 
mustard plaster. Severe headache occasionally requires 
sedatives. 

When the most acute period of acute nephritis has 
passed the patient should have a diet of increased caloric 
value with a low content in proteid and salt. The follow¬ 
ing table is copied from the one furnished by Christian 
in the “Oxford Medicine.” 


Nephritic Diet Salt Poor Calories 2000 


Food 

Amount 

Protein 

Fat 

Carbo¬ 

hydrates 

Calories 


c.c. 

Gms. 

Gms. 

Gms. 


Cream . 

200 

4.40 

80.00 

6.00 

761.60 


Gms. 





Butter. 

60 

.60 

51.00 


461.40 

Bread . 

90 

8.28 

1.17 

47.79 

234.81 

Sugar . 

65 



65.00 

260.00 

Potato. 

100 

2.50 

.10 

20.90 

94.50 

Orange . 

50 

.40 

.10 

5.80 

25.70 

Oatmeal . 

150 

4.20 

.75 

17.25 

92.55 

Lima beans ... 

50 

2.00 

.15 

7.30 

38.55 

Corn . 

100 

2.80 

1.20 

19.00 

98.00 

Pineapple 






(canned) ... 

50 

.20 

.35 

18.20 

76.75 

Peaches 






(canned) ... 

100 

.70 

.10 

10.80 

46.90 

Totals .. 


26.08 

134.92 

218.04 

2190.76 
























96 


CLINICAL MEDICINE FOR NURSES. 


“To the foods given above are added sufficient water, 
tea, coffee, or cocoa to bring the twenty-four hour fluid 
intake up to the level determined on, say 1200 c.c. or 
1500 c.c. per day. An actual sample menu furnished at 


the hospital under the order 
diet is the following. 


Breakfast. 

Baked apple . 50 Gms 

Shredded wheat _ 30 Gms. 

Bread . 30 Gms. 

Coffee . 150 c.c. 

Cream . 40 c.c. 

Sugar . 25 Gms. 

Luncheon. 

Potato . 100 Gms. 

Corn . 100 Gms. 

Bread. 30 Gms. 

Tea. 150 c.c. 

Cream . 20 c.c. 


for a low protein, salt-poor 


Sugar . 

10 

Gms. 

Desserts made of 



pineapple. 

75 

Gms. 

Cream . 

50 

c.c. 

Supper. 



Sliced tomatoes .... 

100 

Gms. 

Macaroni . 

100 

Gms. 

Bread. 

30 

Gms. 

Tea. 

150 

c.c. 

Sugar . 

25 

Gms. 

Cream . 

40 

c.c. 

Canned pears. 

100 

Gms. 

Butter total for day 

60 

Gms. 


This menu, as calculated from food tables, totals 25.6 
Gms. protein, 116.6 Gms. fat, and 247.7 Gms. carbo¬ 
hydrate, yielding 2143.5 calories.” 

When caring for a case of acute nephritis the nurse 
must secure, measure, and record with the greatest care 
the total amount of urine, as this is the most important 
factor concerning which the physician will desire infor¬ 
mation. She must also be keenly alive to the amount of 
edema present, its increase or decrease, and any change 
in the patient that may be suggestive of an approaching 
uremic convulsion. Acute nephritis in its intense forms is 
a fierce fight; and there are few acute conditions in which 
the chances for recovery depend so much upon the mode of 
treatment instituted, and upon the care and faithfulness 
with which the details of this treatment are carried out. 






















CHAPTER XIII. 


CHRONIC NEPHRITIS WITH EDEMA. 

Chronic nephritis with edema differs from acute neph¬ 
ritis in degree only. The process in the kidney is one and 
the same, the causative factors are identical, and, generally 
speaking, the symptoms are also similar, save that they 
are less marked in the chronic than in the acute form. 
It is impossible to draw an absolute dividing line between 
a severe case of chronic nephritis with edema and a conv 
paratively mild case of acute nephritis. 

It follows that a recital of the symptoms must largely 
be a repetition of those cited under acute nephritis. 

Edema is a very constant symptom, and at times is 
very marked. Instead of being universal, it is noticeable 
mainly in the face in the morning, and in the legs in the 
evening, if the patient is up and about. It may become 
the chief complaint, going on to general anasarca, the 
patient finally dying “waterlogged.” 

The urinary changes are similar to those found in acute 
nephritis, save to a lesser degree. The urine is lessened 
in amount, of a rather high specific gravity (1.020 to 
1.025), containing a large amount of albumin and many 
granular and hyaline casts. 

Uremic symptoms of varying intensity are almost al¬ 
ways present. Headache, mental and physical inertia, 
nausea and vomiting are very common. There may be a 
profuse diarrhea. Anemia is generally present, often to 
a marked degree, and despite the increase in actual 
weight (due to edema) the patient looks, and is, emacia¬ 
ted. The heart is usually enlarged, and there is al¬ 
most always dyspnea, partly from heart-strain and 
partly because of the amount of edema. The symptoms 
of acute uremia (q-v.) may occur at any time, but are 

t (97) 


98 


CLINICAL MEDICINE FOR NURSES. 


not as apt to show themselves as in chronic nephritis 
without edema. 

The prognosis is very grave. Recovery is practically 
unknown. The kidneys are permanently damaged. The 
disease runs a course lasting from six months to three 
years, and is characterized by exacerbations, during which 
more and more kidney structure is damaged, and remis¬ 
sions during which some repair seems to take place. Death 
occurs either from the enormous edema, with fluid in the 
peritoneal cavity (ascites), in the pleural cavity (hydro¬ 
thorax), and finally in the lungs (pulmonary edema), 
from uremia, or from some intercurrent disease to which 
the patient, because of lowered resistance, is susceptible. 

Treatment. The principles of treatment are the 
same as those laid down for acute nephritis, i.e., to spare 
the kidneys all possible strain, and to stimulate excretion 
through the other avenues of elimination. Heroic 
measures, however, are not usually necessary. 

General Management. The patient may or may not be 
confined to bed, depending upon the general strength, the 
amount of edema, and particularly upon the comfort of 
the individual. If a patient is more at ease in an arm¬ 
chair than in bed, he is usually allowed to exercise his 
choice. Care should be taken to' protect the patient from 
draughts, from cold, and especially from dampness. 
Great attention to the skin is necessary. Its nutrition is 
frequently markedly interfered with because of the 
edema, and it is very susceptible to infection. Frequent 
warm baths are essential, followed by an alcohol rub and 
liberal powdering with talcum powder. If the patient is 
in bed, the position must frequently be changed, and 
pressure at once removed from, any red or painful area 
of the skin. 


CHRONIC NEPHRITIS WITH EDEMA. 


99 


Elimination through the bowels will, of course, be 
seen to by the attending physician, but the nurse must be 
very careful to call his attention to any signs of con¬ 
stipation, either as regards the number or character of 
the movements. Generally speaking, it is far better for 
the patient to have two or even three stools daily than to 
go a day without a thorough bowel evacuation. The 
amount of catharsis necessary will, of course, be meas¬ 
ured by the general condition of the patient. 

Diuretics are almost always employed, and have a great 
field of usefulness in these cases. Whether requested or 
not, the nurse should always keep a charted record of 
the total twenty-four-hour urine, so that it can at once 
be turned to for reference. A hot pack or two per week 
often proves of benefit, both in aiding elimination through 
the skin and in keeping it in good condition. 

Diet. Formerly, patients with chronic nephritis with 
edema were very markedly restricted as to their diet, 
especially as to variety, and were fed milk ! milk!! milk !!! 
until their very lives became a burden. More recently, 
however, it has been found that these patients do quite 
as well on a more liberal allowance. The patient’s pro- 
teid intake must be restricted—how much is to be de¬ 
termined in the individual case, but as a rule not over 
80 to 100 Gm. are to be taken in twenty-four hours. 
Broadly speaking, the fats and carbohydrates can be 
freely taken, comprising, among other things, well- 
cooked green vegetables, root vegetables, cereals, fruits 
and simple desserts. Sugar may be given freely. Spices, 
condiments, alcohol, meat soups and heavy meats are to 
be avoided. It has been found, however, that a lamb 
chop or two, or a small piece of steak twice a week, do 
no harm, and materially help the patient’s appetite and 


100 


CLINICAL MEDICINE FOR NURSES. 


general morale. The dietary table given in the chapter 
on Acute Nephritis will be found useful for these cases of 
chronic nephritis with edema. Its scope can be widened 
according to individual needs. 

Restriction of Fluids .—This depends largely upon the 
amount of edema. If there is much dropsy, it is evi¬ 
dent that water does not pass freely through the kidneys, 
and in such cases the amount of fluid intake is limited. 
If edema is very slight, or absent, it is frequently cus¬ 
tomary to give the patient enough water to bring the 
total amount of urine in twenty-four hours up to about 
3 pints, or 50 ounces. Water is one of the best diuretics, 
and in suitable cases is invaluable. 

Salt Restriction. In many cases of chronic nephritis 
with edema the kidneys do not excrete salt (sodium chlo¬ 
ride) satisfactorily. Almost everyone eats much more 
salt with food than is necessary for use in the body, and 
the excess must be eliminated through the kidneys. In 
cases of nephritis with edema, many have adopted the 
rule to reduce the salt intake to 2 Gm. (30 grains) in 
twenty-four hours. This is often at first a considerable 
hardship to the patient, but it is frequently necessary to 
enforce it in order to get rid of the edema. 

Further Measures. If ascites or hydrothorax are pres¬ 
ent, the fluid is generally withdrawn.by tapping. Insom¬ 
nia must receive appropriate treatment by means of hyp¬ 
notics and sedatives. Iron in some form is usually given 
for the anemia. To the highest degree must the treat¬ 
ment of chronic nephritis with edema be one of individu¬ 
alization; the conscientious nurse, with a knowledge of 
what is being attempted, and why it is being tried, will be 
of inestimable help to both physician and patient. 


o .* 


CHAPTER XIV. 


CHRONIC NEPHRITIS WITHOUT EDEMA 
AND ARTERIOSCLEROSIS. 
(Cardiovascular-renal Disease.) 

While in textbooks on medicine chronic nephritis 
without edema and arteriosclerosis are dealt with in separ¬ 
ate chapters, for the sake of simplification it has seemed 
best to consider them together, and in that connection to 
dwell also upon the relationship borne and the part played 
by the heart, this triple combination being recognized and 
often spoken of as cardiovascular-renal disease. 

This disease is of very frequent occurrence, and is in 
fact one of the most common conditions seen in elderly 
persons. It gives rise to a great number of symptoms, 
but usually one of the elements (the heart, the blood¬ 
vessels, or the kidneys) is more prominent than either of 
the other two, and the majority of symptoms complained 
of or observed can be laid at the door of one of the three 
units going to make up the pathological condition. 

Chronic nephritis without edema and arteriosclerosis are 
so closely interwoven, and their causative factors so simi¬ 
lar, that one is hardly ever seen without the other, and the 
almost invariable rise in blood-pressure at once throws 
an added strain on the heart, to which that organ, though 
it may bear up for a time, must in the end assuredly 
succumb. 

The causes leading up to chronic nephritis without 
edema and arteriosclerosis are: 


(101) 


102 


clinical Medicine for nurses. 


1. Age. Over 55 years every individual undergoes 
changes presently to be described, which to a greater or 
lesser degree affect the kidneys and the arteries. 

2. Alcohol, especially when used regularly over a long 
period of years, even if never to excess. 

3. Overeating, especially when this is combined, as it 
so often is, with a sedentary life, an overplus of alcohol 
and tobacco, too great a dependence upon the luxuries of 
life, and insufficient exercise. 

4. Faulty metabolism, such as gout and diabetes. 

5. Syphilis. 

Pathology. The essential feature in bringing about 
a condition of chronic nephritis without edema and arterio¬ 
sclerosis is the establishment of a process of fibrosis in 
the human body. By fibrosis is meant the gradual trans¬ 
formation of normal tissue into dense, firm, inelastic 
fibrous tissue. This process attacks mainly the kidneys 
and the arteries. It is one of the signs of advancing 
years, one of the signals that the human machine has 
seen its best days, has done its best work, and is wearing 
out. Many cases of general fibrosis occur simply as a 
result of age, none of the other causative factors playing 
any role whatsoever. 

The kidneys are small, dark, mottled, and the capsule, 
instead of peeling off easily, is everywhere densely ad¬ 
herent, and when stripped brings away with it small 
pieces of kidney tissue. 

Microscopic evidences of fibrous tissue formation 
while visible in the uriniferous tubules, are most marked 
in the glomeruli and in the interstitial tissue. The glom¬ 
eruli are largely destroyed, being in many instances re¬ 
duced to mere fibrous tufts with no traces of capillaries, 
epithelium, or capsule of Bowman left. The interstitial 


CHRONIC NEPHRITIS WITHOUT EDEMA. 103 

tissue appears greatly increased in amount, the urinifer- 
ous tubules are relatively few, and the cells lining them 
are flattened out and show evidences of degeneration. 

The arteries suffer most in their middle coat (the 
media). It is here that normally the elastic fibres are 



Fig. 5.—Chronic nephritis, atrophied kidney, vascular type. 
(From a “Handbook of Pathological Anatomy and Histology,” 
by Delafield and Prudden. Courtesy of Wm. Wood & Co., 
publishers.) 

situated that allow the artery to expand with each beat 
of the pulse, and that, more important still, by their re¬ 
coil help the heart to such a great extent to force the 
blood-current along. These elastic fibres are transformed 
to a greater or less extent (according to the severity of 


104 


CLINICAL MEDICINE FOR NURSES. 


the process) into fibrous tissue, so that the vessel wall 
becomes comparatively rigid. In addition, deposits of 
lime salts occur in the arterial walls, sometimes to such 
an extent that the radial artery, when rolled under the 
finger, feels like a pipe stem. 

It will readily be seen that with unyielding, inelastic 
arteries blood-pressure must rise, and with heightened 
blood-pressure the heart has to pump against an abnor¬ 
mally great resistance. This results in increased work 
on the part of the heart, showing itself by hypertrophy 
of that organ, especially of the left ventricle. In time, 
however, the heart shows signs of failing, and symptoms 
of cardiac dilatation make their appearance. 

Symptoms. 1 .Urinary. The amount of urine is greatly 
increased, and one of the first symptoms noted by the 
patient (and rarely complained of) is the necessity of 
arising two or three times during the night to empty the 
bladder. The total urine voided in twenty-four hours is 
usually from 2% to 3% quarts (1 % quarts being ap¬ 
proximately normal). The specific gravity is very low, 
usually under 1.010. There may or may not be albumin 
present, and if found it is usually very slight in amount. 
On microscopical examination a few hyaline casts may 
be seen. It is impossible in these cases to tell from an 
ordinary urinary examination the extent of damage to the 
kidney, and recourse must be had to the tests for kidney 
function ( q.v .). 

2. Toxic. Signs of uremia may, and usually do, show 
themselves. It is not uncommon for patients with car¬ 
diovascular-renal disease to suddenly suffer from an 
attack of acute uremia, with convulsions, suppression of 
urine, etc. More frequently, however, are seen the signs 
of chronic uremia, which are an indication that the kid- 


CHRONIC NEPHRITIS WITHOUT EDEMA. 105 

neys are eliminating insufficiently, and that poisons in the 
shape of waste products are being gradually accumulated 
within the system. These symptoms are: headache 
(especially in the morning), a coated tongue, some con¬ 
stipation, slight drowsiness, dizziness, mental depression, 
and a slight mental dullness. 

3. Cardiac. The patient frequently suffers from pal¬ 
pitation, and dyspnea is very common, especially on slight 
exertion. Some cough is frequent and a chronic bron¬ 
chitis, accompanied by much “wheezing,” often is present 
as a result of heart weakness. 

Sudden edema of the lungs may occur. Hemorrhages, 
especially nosebleed and blood in the urine, are frequent 
as a result of the giving way of small vessels because of 
the heightened blood-pressure. Apoplexy is a frequent 
occurrence, due to the rupture of a blood-vessel in the 
brain, because of the combination of inelastic walls and 
heightened blood-pressure. 

Gastric and digestive disturbances are very common, 
loss of appetite, nausea, vomiting and constipation being 
most prominent. 

Edema is absent save if an attack of acute nephritis 
occurs, which is not infrequently the case. The blood- 
pressure is almost invariably raised, in some cases to 
alarming heights. 

It will be seen that the symptoms of this disease of 
triple origin are so numerous that an accurate picture of 
the condition is very difficult to obtain, because of the 
number of elements involved. Probably no case will ex¬ 
hibit all the symptoms, and, as previously mentioned, 
those symptoms referable to one of the three elements at 
fault will usually dominate the scene. 


106 


CLINICAL MEDICINE FOR NURSES. 


Prognosis. The outlook is bad, as far as recovery 
is concerned. Permanent tissue changes have taken place 
which cannot be cured, and while by careful attention to 
hygiene, diet, and special symptoms, the patient’s life can 
be considerably prolonged, and made in many instances 
very comfortable, yet in the end the fight is bound to be 
a losing one. 

Treatment. The objects of treatment are threefold: 

1. To spare the kidneys as much as possible. 

2. To spare the heart as much as possible by reducing 

blood-pressure. 

3. To relieve symptoms as they arise. 

1. In attempting to spare the kidneys, the diet is essen¬ 
tially the same as that in chronic nephritis with edema, 
save that reduction of salt is not usually necessary, for 
edema is rare, and when it appears, is usually of cardiac 
origin or the result of an acute nephritis. Proteid must 
be given sparingly, not more than 80 to 100 Gm. in 
twenty-four hours. 

Elimination through the bowels and skin is important, 
the latter being often well secured by a course of sweats 
every few weeks. 

2. In reduction of blood-pressure sweats work well, as 
abnormal tension is due, in part at least, to the kidneys. 
In addition, drugs are often given whose action is to 
lower blood-pressure. These drugs are known as vaso¬ 
dilators, because they cause the blood-vessels to dilate or 
expand, and therefore allow the contained blood to be 
under less pressure. 

The main drugs used are: 

(a) Amyl nitrite. 

(b) Nitroglycerin. 

(c) Sodium nitrite. 


CHRONIC NEPHRITIS WITHOUT EDEMA. 107 


Of . these, amyl nitrite acts most rapidly, but its effect 
is violent, often very uncomfortable to the patient, and 
very transient in duration. Nitroglycerin acts rapidly, 
but must be frequently repeated, as its action is also 
transient, and, when given in large doses, is apt to cause 
severe headache. Sodium nitrite acts more slowly than 
the two preceding, but its action is far more sustained, 
and it does not give rise to the disagreeable symptoms 
caused by the other two drugs. In addition, potassium 
iodide is very frequently given, though it has no power 
to reduce blood-pressure. The dosage and frequency of 
administration of these drugs will, of course, be deter¬ 
mined by the-attending physician. At the present time 
there is far less indication to lower blood-pressure by 
means of drugs than formerly. In many instances the 
desired effect is not seen and blood-pressure does not fall. 
In many other cases blood-pressure falls but the patient 
feels no better and even may often feel worse as a re¬ 
sult. We are coming more and more to recognize hyper¬ 
tension as in many ways a compensatory phenomenon 
and also to see that radical alterations in blood-pressure 
are by no means always desirable. 

3. The relief of individual symptoms has nothing to 
do with the actual treatment of the condition under con¬ 
sideration. These symptoms are so many and varied that 
a host of methods are in use, each physician having his 
preference. Sedatives of one kind or another will usually 
have to be employed, and in the vast majority of cases 
morphia will finally be resorted to, especially for the noc¬ 
turnal dyspnea, which is often so distressing. During 
the earlier stages of the disease the patient should not be 
kept in bed, but encouraged to take mild exercise, always 
carefully abstaining from overfatigue. For such patient 


108 


CLINICAL MEDICINE FOR NURSES. 


golf over a flat course is ideal. The care of the skin and 
bowels is all-important. Early and moderately advanced 
cases can usually do work, if that work is not manual and 
violent. Such cases will not need a nurse. The nurse 
sees these unfortunates when their days of activity are 
behind them, and when the exhausted and rapidly failing 
vital organs can no longer cope with the work demanded 
of them. 


CHAPTER XV. 


TESTS OF KIDNEY EFFICIENCY. 

(Renal Function Tests.) 

Within the last fifteen years much light has been shed 
upon the workings of the organs of our bodies, and 
methods have been devised to test their working powers 
or functional efficiency. In no organ has this power'been 
the subject of more investigation than in the kidney, and 
in the case of no other organ have the results been as 
satisfactory and as easily practicable for everyday use. 
Fifteen years ago, if on a careful urinary examination the 
specific gravity was normal, and no albumin, sugar, or 
casts were found, it was taken for granted that the kid¬ 
neys were in normal condition. Today the situation has 
been complicated by the knowledge that seriously dis¬ 
eased kidneys may secrete a urine by no means propor¬ 
tionately abnormal. This insufficiency of excretion on 
the part of the kidneys has been made plain by the dis¬ 
covery of the renal function tests. 

The nurse, of course, will not be called upon to make 
these tests; neither is it necessary that she should know 
their theoretical foundations. The nurse will, however, 
assuredly care for many patients in whom these tests will 
be made, and she should, in a general way, appreciate 
their significance and understand their mode of applica¬ 
tion in order to more intelligently co-operate with the 
physician in his work. There are many tests for esti¬ 
mating kidney function, no one of which, alone, can 

(109) 


110 


CLINICAL MEDICINE FOR NURSES. 


give a complete picture of the working powers of the 
kidney. Several of these tests are very complicated, re¬ 
quire a laboratory technician for their performance, and 
can never become a routine in general practice. There 
are, however, two tests that can be performed with great 
ease, and that often give valuable information as to the 
functionating power of the kidneys. 

These two tests are the ones most used by physicians 
in their practice, and the nurse should be familiar with 
the modes of procedure. 

These tests are: 

(1) Phenolsulphonephthalein test. 

(2) Specific gravity test. 

1. Phenolsulphonephthalein test (commonly known as 
the phthalein test). 

This test is based upon the ability of the kidney to 
excrete a certain amount of this particular dye in a given 
length of time.. The technique of performing the test is 
very simple. There are many slight modifications, the 
following being sufficiently accurate for general clinical 
work. 

Fifteen minutes before making the test the patient is 
given 400 c.c. of water to drink. Immediately before 
beginning the test the bladder is emptied. One c.c. of a 
1 per cent, solution of phenolsulphonephthalein (a bril¬ 
liant red dye that is put up in ampoules specially for this 
test) is then injected into the muscles of the back. The 
patient is given no food or drink, and exactly one hour 
and ten minutes after receiving the injection empties 
the bladder, the entire amount of urine voided being 
placed in a bottle labeled thus: “1st hour.” In exactly 
one hour more the bladder is again emptied, and the 
urine voided is placed in a bottle labeled: “2d hour.” The 


TESTS OF KIDNEY EFFICIENCY. Ill 

test, as far as the patient is concerned, is then at an 
end. 

The urine in the bottle labeled “1st hour” is poured 
into a 1000-c.c. graduate, and, irrespective of its amount, 
water is added up to 1000 c.c. A few drops of 40 per 
cent, sodium hydrate are added, which causes the diluted 
urine to become pink or red, according to the amount of 
the dye present. A small portion of the contents of the 
graduate is then taken and compared with a standard 
scale in an instrument known as a colorimeter, the 
counterpart of the color of the urine being found on the 
scale, and the percentage of the dye excreted, read off, 
and recorded. The contents of the bottle labeled “2d 
hour” are similarly dealt with, and the percentage of the 
dye excreted during the first and second hours are added 
together. 

Normal kidneys will excrete from 60 to 80 per cent, of 
the dye within two hours. Any percentage below 50 de¬ 
notes that the kidneys are under-functioning, and when 
percentages of 35 and less are reached the patient is in 
danger of an attack of uremia, even though there may 
be no symptoms of that condition present. 

2. Specific Gravity Test. This very simple procedure 
shows the specific gravity of the urine at various hours 
during the day, demonstrates the presence or absence of 
nocturnal polyuria, and sets forth the fact whether the 
specific gravity of night urine is higher than that of day 
urine (normal) or whether it is the same (usually abnor¬ 
mal). The nurse can carry out this test for the physi¬ 
cian with the greatest ease, the only accessories required 
being a 500 c.c. graduate and a specific gravity float 
(urinometer). 

In cases where very great accuracy is desired, a defi- 


112 


CLINICAL MEDICINE FOR NURSES. 


nite “renal test-diet” is given. This diet has been care¬ 
fully worked out by Dr. H. O. Mosenthal at the Johns 
Hopkins Hospital. When this is used, the exact amount 
of salt given is measured, and that not used is deducted 
from the total. For ordinary clinical purposes such ac¬ 
curacy is not essential, as is shown by the following 
quotation from one of Dr. Mosenthal’s articles: 

“In private practice it would only be necessary to ask 
the patient to eat three full meals a day, and write down 
the approximate quantities (as: 1 cup of coffee, 2 slices 
of toast, 2 tablespoonfuls of oatmeal, etc.), in order to be 
certain that the diet for the day contained a sufficient 
quantity of the diuretic materials of ordinary food to 
make an adequate demand on the kidney to test renal 
function. 

“It is extremely desirable to insist that, since the 
food as found in most households suffices to carry 
out these tests, and the procedure is not a complicated 
one, it need not be confined to hospitals and patients who 
can afford private nurses.” 

Technique of the Test. No food or fluid to be given 
between meals, and none between 8 p.m. and 8 a.m. 
Patient empties bladder every two hours—at 8 a.m., 10 
a.m., 12 noon, 2 p.m., 4 p.m., 6 p.m., and 8 p.m. If pos¬ 
sible, patient is to go from 8 p.m. to 8 a.m. without void¬ 
ing. If this is not possible, all urine voided between 8 
p.m. and 8 a.m. is to be collected and mixed before tak¬ 
ing specific gravity. Every voiding during the day is to 
be measured, and the specific gravity taken, and both 
findings recorded. 

The following table is taken from Dr. Mosenthal’s 
article and represents the findings in a normal in¬ 
dividual : 


TESTS OF KIDNEY EFFICIENCY. 


113 


Time of day 

Urine 

c.c. 

Sp. G. 

8 to 10 

153 

1.016 

10 to 12 

156 

1.019 

12 to 2 

194 

1.012 

2 to 4 

260 

1.014 

4 to 6 

114 

1.020 

6 to 8 

238 

1.010 

Total day 

1115 


Night, 8 to 8 

375 

1.020 

Total, 24 hours 

1490 


To be noted are: The variations occurring in the fluid 

output and in the specific gravity, which, generally speak- 

ing, are in inverse -ratio, 

i.e., the greater the amount of 

urine the lower the specific gravity; 

the small amount 

of night urine with high specific gravity. 

In contrast to the preceding, the 

following table is 

shown, taken from an advanced case of chronic nephritis 

without edema: 




Urine 


Time of day 

c.c. 

Sp. G. 

8 to 10 

24 

1.005 

10 to 12 

106 

1.006 

12 to 2 

82 

1.007 

2 to 4 

83 

1.008 

4 to 6 

0 


6 to 8 

230 

1.008 

Total day 

525 


Night 

1140 

1.007 

Total, 24 hours 

1665 



To be noted are: the low specific gravity, with but 
(very little variation (so-called “fixed” specific gravity), 
the small amount of day urine, and the large amount of 
night urine with a low specific gravity. 

8 











114 


CLINICAL MEDICINE FOR NURSES. 


This test is very valuable, and, taken in conjunction 
with the phthalein test, gives some working idea of the 
functional ability of the kidneys. It must not, however, 
be supposed that these tests are in any way infallible. 
Many times a patient with acute nephritis, with an out¬ 
put of only some 20 ounces of urine in twenty-four hours 
will show an almost or wholly normal phthalein excretion. 
One performance of the phthalein test in a patient is not 
worth much. It is only by its repeated use, and by its 
correlation with the general clinical condition of the pa¬ 
tient that results of any value can be obtained and even 
then, the percentage of error in the interpretation of the 
test is large. The specific gravity test is of distinct diag¬ 
nostic value, but of no great importance in estimating the 
progress of a given case. 


CHAPTER XVI. 


CEREBRAL HEMORRHAGE (APOPLEXY) 

AND CEREBRAL THROMBOSIS. 

Nature of the Conditions. By cerebral hemorrhage is 
meant the escape of blood into the tissue of the brain by 
the bursting of one of its blood-vessels. 

By cerebral thrombosis is meant the stopping up of 
one or more of the vessels of the brain by a clot or 
thrombus, thus depriving of its blood-supply the area of 
brain nourished by the occluded vessel. 

These conditions occur usually in middle life or in old 
age, and have as their one great cause, arteriosclerosis. 
High blood-pressure, coupled with inelastic, unyielding 
vessel walls, predispose to hemorrhage, while low blood- 
pressure and the roughened interior of arteriosclerotic 
vessels result frequently in the formation of thrombi or 
clots. 

Cerebral hemorrhage and thrombosis may occur in the 
comparatively young (30 to 40) if the arteries are 
sclerotic, and this is especially apt to be the case in 
syphilitic subjects. 

Cerebral Hemorrhage. 

Symptoms. The symptoms vary greatly in degree, 
and depend upon the location and the size of the hemor¬ 
rhage. If the hemorrhage is very large, the patient may 
drop dead. In less severe cases the “stroke’' may cause 
unconsciousness, persisting for several days, accom¬ 
panied by stertorous breathing, slow pulse, and a hemi¬ 
plegia, i.e., complete paralysis of one-half the body, ex- 

( 115 ) 


116 


CLINICAL MEDICINE FOR NURSES. 


tending from head to heel. The paralysis always occurs 
on the opposite side from the hemorrhage, due to the 
crossing of the nerve fibres from one side of the brain 
to the other. One side of the face is paralyzed, the smile 
is crooked, the corner of the mouth being drawn over to¬ 
ward the sound side. The tongue when protruded points 
away from the side of paralysis. The arm, hand, thigh, 
leg, and foot on one side are incapable of any motion, 
and may also feel numb, or else be notably insensitive to 
touch. Depending upon the site of the hemorrhage, 
there may be various disturbances of speech, known as 
aphasia, .the patient being unable to utter the word de¬ 
sired, unable to remember words, using the wrong word, 
e.g., saying “hat” for “breakfast,” “shoe” for “tooth¬ 
brush,” etc., thus being wholly unintelligible. The func¬ 
tions of rectum and bladder may be interfered with, con¬ 
stipation being present or else both urine and feces being 
voided involuntarily. All symptoms depend upon the loca¬ 
tion, and extent of destroyed or damaged brain tissue. 

In milder cases the paralysis may be more localized, 
one arm, one leg, or the face only being affected, and 
at the time of the “stroke” there may be no uncon¬ 
sciousness. 

The course of the disease is subject to great varia¬ 
tions. Complete recovery is not to be expected in a 
hemorrhage of any size, as a certain portion of brain- 
tissue is always permanently destroyed. Usually there 
is some improvement for a while after the “stroke,” as 
portions of the brain affected slightly by the hemorrhage, 
but not destroyed, regain and resume their function. A 
period eventually is reached where no further improve¬ 
ment takes place, and the patient continues for an in¬ 
definite period in his paralyzed condition. Death occurs 


CEREBRAL HEMORRHAGE AND THROMBOSIS. 117 


from successive “strokes” or hemorrhages, from exhaus¬ 
tion, from infection of bladder and kidneys, or from 
bed-sores, which are very apt to occur, as the nutrition 
of the skin is often interfered with. 

Treatment. The patient suffering from an apoplectic 
stroke is to be put to bed, with the head high and the feet 
low. One of the objects of treatment is to draw as much 
blood as possible away from the brain. For this purpose 
an ice-bag may be placed on the head, and heat applied to 
the feet. Free catharsis is desirable, in order to abstract 
blood and to lower blood-pressure. To obtain many 
bowel movements in an unconscious patient croton oil is 
often used. Drugs to quiet the heart’s action and reduce 
blood-pressure, such as aconite and veratrum viride, are 
frequently given. An ice-bag over the heart is often 
effective. Some cases are benefited by bleeding 12 to 16 
ounces from a vein (venesection). 

The nurse must be careful to frequently change the 
patient’s position in order to lessen the likelihood of 
hypostatic pneumonia, as well as to lessen continued 
pressure upon any one spot on the skin. She must also 
pay particular attention to keeping the skin clean and 
dry (which is often difficult because of the involuntary 
movements), as bed-sores are apt to develop, and, once 
present, to spread rapidly, and sometimes cause the 
death of the patient. The nurse must also report to the 
physician whether a sufficient amount of urine is being 
voided, as these patients often allow the bladder to be¬ 
come overdistended, and only the “overflow” of urine is 
passed. 

For the frequent restlessness, especially at night, seda¬ 
tives are necessary, such as the bromides and chloral, and 
morphia must often be resorted to. 


118 


CLINICAL MEDICINE FOR NURSES. 


Cerebral Thrombosis. 

The symptoms of cerebral thrombosis are neither as 
marked nor as striking as those of cerebral hemorrhage, 
though, in the end, the damage done may be fully as 
great. If a vessel is gradually stopped up, the function of 
that part of the brain which it supplies is, of course, grad¬ 
ually interfered with. The symptoms depend entirely 
upon the location of the thrombosis. There may be 
weakness, numbness, or a sense of “pins and needles” in 
a hand or arm; dizziness; thick, difficult speech, and any 
of the different forms of aphasia. Loss of consciousness 
is not the rule, though it may occur if the occluded vessel 
is very large. The thrombotic process usually spreads, so 
that eventually hemiplegia may result. 

As in the case of apoplexy, perfect recovery cannot 
occur, as some portion of the brain is permanently dam¬ 
aged. If the process does not spread, certain parts of the 
affected brain-tissue may regain their function by re¬ 
ceiving blood from other vessels than the one that has 
become occluded (collateral circulation), but a certain 
amount of damage is irreparable. 

Treatment. As these cases are usually associated 
with low blood-pressure, the object of treatment is the 
opposite of that advocated for cerebral hemorrhage, i.e., 
it is desired to drive blood to the brain. The head should 
be low and the feet elevated. Heat over the heart is ad¬ 
visable, and profuse catharsis is usually not practised. 
Stimulation is often indicated, and, in addition, drugs to 
prevent constriction of the cerebral blood-vessels, of 
which nitroglycerin is the best example. The remainder 
of the management of the patient differs in no way from 
that outlined under cerebral hemorrhage. 


CHAPTER XVII. 


PLEURISY. 

(Dry and With Effusion.) 


By pleurisy is meant inflammation of the pleura, which 
is the serous membrane that surrounds the lung. 

The pleura is formed of two layers, one lying directly 
against the lungs (the visceral pleura), the other lying 
between the visceral pleura and the inner surface of the 



Trachea. 


.Main Bronchus 


■ —Pleoral Ccmfcj 

■ |- 

j -VParifclal PletnNX 
—Vfjcer a) Pleura 


Fig. 6.—Diagram of pleural sacs. 


ribs, and known as the parietal pleura. These two layers 
of pleura become continuous with each other, above and 
below the hilus or root of the lung. (See diagram.) 

The parietal and visceral layers of pleura are con¬ 
stantly in contact, a few drops of fluid being found be¬ 
tween them for purposes of lubrication. The so-called 
“pleural cavity” lies between the parietal and visceral 
layers. In health there is no “space” or “cavity,” the two 
layers being closely applied one against the other. Both 
pleural sacs are wholly and entirely separate and distinct, 
one from the other, there being one for each lung. 


( 119 ) 






120 


CLINICAL MEDICINE. FOR NURSES. 


It is often very difficult for nurses to appreciate what 
is meant by the “pleural cavity.” The following simile 
may be of assistance. 

If the stopper is removed from' a hot-water bottle, 
if the bottle is then rolled up so as to drive out all the 
air, and if then the stopper is tightly screwed in, it will 
be impossible to separate the two layers of rubber form¬ 
ing the hot-water bottle, because of the pressure of air 
from the outside. Yet it would be easy enough to figure 
to one’s self a “cavity” within the hot-water bottle, if 
only air or water could be gotten in between the two 
layers. It is in the same sense that the pleural “cavity” 
exists. Normally the layers are as close to each other 
as the sides of the hot-water bottle, differing from it 
in that they slide against each other with every respira¬ 
tory movement of the lungs. If fluid or air appears be¬ 
tween the layers of the pleura they are forced apart and 
the “pleural cavity,” from being a feat of the imagina¬ 
tion, becomes an accomplished fact. 

It is important to understand this question of the 
pleural cavity in order to appreciate conditions in pleurisy 
with effusion, and in pneumothorax, whether spontaneous 
or artificial. (See last section in chapter on Tuber¬ 
culosis.) 

There are two varieties of pleurisy: 

(1) Dry pleurisy. 

(2) Pleurisy with effusion. 

1. Dry Pleurisy. In dry pleurisy there is congestion 
of the two layers of the membrane over the site of in¬ 
flammation, and minute threads of fibrin extend from 
one layer of the pleura to the other. When the act of 
respiration takes place, instead of gliding smoothly over 
each other, the two pleural surfaces grate, the fibrin 


PLEURISY. 


121 


strands stretch and break, and, as the pleura is very richly 
supplied with nerves, intense pain is felt over the in¬ 
flamed area. 

Etiological factors. 

(1) Cold, especially in connection with getting wet. 

(2) Trauma, e.g. } a blow or a kick. 

(3) Infectious diseases, especially: 

(a) Lobar pneumonia (dry pleurisy always 

present). 

(b) Tuberculosis; 90 per cent, of idiopathic 

cases of pleurisy are of tuberculous 
origin. 

Symptoms. 

Pain. Sharp, knife-like, lancinating. May be localized 
or spread over quite a wide area. Usually most marked 
at the side of the chest and toward the base of the lung. 
The pain is increased by deep breathing, and is often 
severe enough to “cut off the breath.” It is also increased 
by laughing, sneezing, coughing, blowing the nose, or 
any inspiratory or expiratory effort. 

Dyspnea. Due to the pain, which necessitates frequent 
short breaths. Sometimes the dyspnea is so intense as to 
produce a slight grade of cyanosis. It has often been 
noticed that a hypodermic of morphia, by relieving the 
pain and permitting deeper breaths, will wholly dissipate 
the cyanosis. 

Fever. Usually low—under 101°. Many cases show 
no fever. Some have as much as 102°. 

Treatment. 

Drugs. If the pain is bad, codeine, either by mouth or 
by hypodermic, usually gives relief, though not infre¬ 
quently morphia is necessary. Some patients are bene¬ 
fited by acetylsalicylic acid (aspirin). 


122 


CLINICAL MEDICINE FOR NURSES. 


Local Measures. Some form of counterirritation is 
almost always used. The means most employed are: 

(1) Heat (hot-water bottle). 

(2) Iodine. 

(3) Mustard plaster. 

(4) Antiphlogistine. 

(5) Cantharides blister. 

Strapping with adhesive plaster: 

Strapping. Incorrect strapping is useless. The straps 
must be put on tight, and must remain tight if their 
action, to act as a splint and to limit motion, is to be 
obtained. 

Adherence to the following simple suggestions will en¬ 
sure tight and correct strapping: 

( a ) Use 2U>-inch or 3-inch adhesive. 

( b ) Cut strips so that they will reach a little more 

than half way around the body, from a little 
beyond the sternum to a little beyond the 
spine. Unless the ends of the adhesive strips 
are firmly anchored to the “fixed” points of 
the thorax (the sternum and the spine) they 
cannot remain tight. 

(c) Always have the patient sitting or standing 

when strapping is to be done, with hand on 
side to be strapped resting on top of head. 

( d ) If the chest is hairy, shave it. 

( e ) Tell th6 patient to exhale (empty the chest), 

and to hold it emptied during the application 
of each strap. 

(/) Bring straps above and below the nipple in 
women, and in men protect nipple with a 
piece of cotton. 


PLEURISY. 


123 


Straps should not be left in place more than 
four or five days, because of the irritation to 
the underlying skin. 

2. Pleurisy with Effusion. At times an exudate is 
poured out from the surfaces of the pleural layers, and 
fluid appears in the “pleural cavity.” The amount of this 
fluid varies greatly. There may be an ounce or so, or as 
much as three quarts. The fluid in typical cases is a 
clear straw color. It may, however, be turbid from the 
presence of pus, or it may be bloody. The latter condi¬ 
tion occurs most frequently in malignant disease of the 
lungs and mediastinum. 

Symptoms. Pleurisy with effusion is almost always 
/preceded by dry pleurisy, with its characteristic symp¬ 
toms. With the development of fluid there is: 

1. Cessation of pain, due to the mechanical separation 
of the pleural layers by the accumulating fluid. This rule 
has frequent exceptions but the knife-like pain is usually 
transformed into a dull and continuous ache. 

2. Moderate fever —101° to 103°. 

3. Increasing Dyspnea. As more and more fluid col¬ 
lects, the lung on 1 that side is markedly compressed, the 
heart is displaced to right or left (away from the fluid), 
as the case may be, and any physical exertion greatly in¬ 
creases dyspnea. The patient is often comfortable only 
in the erect posture. Cyanosis may set in. 

4. Sense of Weight. A heaviness is complained of on 
the side where the fluid is to be found. As a chest two- 
thirds full of fluid contains about four or five pounds of 
water, thi9 is not to be wondered at. Patients frequently 
complain of feeling the fluid “slosh” about whenever they 
change their position. 


124 


CLINICAL MEDICINE FOR NURSES. 


5. Loss of appetite , nausea and vomiting; especially in 
left-sided cases, because there is nothing between the 
fluid and the stomach but the left leaf of the diaphragm. 
The weight of the fluid constantly pressing on the stom¬ 
ach causes annoying symptoms. 

Treatment. 

Bed during the febrile period, light diet, and attention 
to the bowels. Many effusions need no interference, and, 
in time, become absorbed. Many physicians follow the 
rule not to interfere with a pleuritic effusion if it does 
not inconvenience the patient, as shown by fever, dyspnea 
and cyanosis. 

If it is decided to try to remove the effusion, there are 
two methods, of procedure: 

1. To facilitate and hasten absorption by the giving of 
large doses of saline cathartics, which abstract fluid from 
the body. This method is not much in use at present. 

2. Paracentesis, i.e., tapping. 

The nurse should have the following ready and sterile: 

1. Two c.c. Luer hypodermic syringe with small needle. 

2. Ten c.c. 0.5 per cent, novocain solution. 

3. One small knife with sharp slender point. 

4. One large paracentesis needle. 

5. One 50 c.c. Luer syringe with rubber connection to fit 

paracentesis needle. 

6. Two sterile towels. 

7. Sterile cotton. 

8. Small pieces of sterile gauze. 

9. Collodion. 

10. Alcohol or iodine. 

11. A pair of rubber gloves. 

The space selected is usually the seventh intercostal 
space, in either the posterior axillary or the mid-scapular 


PLEURISY. 


125 


lines. The patient is usually placed in a sitting posture, 
propped against pillows. If there is much fluid, the 
physician often finds it advisable to withdraw not more 
than 1000 c.c. at one time, as the change in pressure within 
the chest, or the change in position of the heart, may bring 
about unpleasant symptoms. Tapping in the vast majority 
of instances is a harmless procedure. At any sign of 
faintness, nausea, uncontrollable cough or profuse, frothy 
expectoration on the part of the patient, it is usual to stop 
the procedure. If only 1000 c.c. are drawn off, the re¬ 
mainder of the fluid may be aspirated in a few days. 

Sometimes one tapping will suffice. Sometimes the 
fluid re-collects, and successive tappings are required. 
Latterly, some physicians have adopted the practice of 
removing the fluid and substituting air. (See section on 
Artificial Pneumothorax in chapter on Tuberculosis.) 


CHAPTER XVIII. 


. t.fi ». 

LOBAR PNEUMONIA. 

Definition. “An infectious disease characterized by 
inflammation of the lungs, toxaemia of varying intensity, 
and a fever that terminates abruptly by crisis” (Osier). 

Etiology. The causative factor in lobar pneumonia 
is the pneumococcus of Frankel and Weichselbaum, 
which was discovered in 1884. 

Contributory causative factors: 

1. Geographical. Pneumonia occurs in all climates, 
but is less frequent in the arctic and antarctic regions 
and near the equator, and most frequent in the temperate 
2ones. 

2. Season. The winter and spring months show the 
largest number of cases of pneumonia. 

3. Cold. Not in itself enough to cause pneumonia. 
For instance, there were but few cases of pneumonia re¬ 
corded during the celebrated retreat of the French army 
from Moscow in the dead of winter in 1812. Cold asso¬ 
ciated with getting wet is a very potent factor in bring¬ 
ing about the disease. Immersion in water, getting wet 
and chilled, and being unable to change one’s clothes 
promptly, often determines the onset of pneumonia. 

4. Injury to the chest, such as a blow or a kick, is 
unquestionably a factor at times in the causation of 
pneumonia. 

5. Inhalation. Especially of ether, and after tra¬ 
cheotomy, as then the defensive mechanism of the upper 
air-passages is done away with. 

(126) 


LOBAR PNEUMONIA. 


127 

6. Alcoholism. A powerful factor in reducing bodily 
resistance, and predisposing to the disease. Alcoholism, 
wet, and exposure to cold, so often found in combination, 
furnish a fertile ground for the development of pneu¬ 
monia. 

7. Age. While occurring at all times of life, individ¬ 
uals between 20 and 30 are most prone to the disease. 
Thus, among 32,681 cases, 8041, or 24.6 per cent., oc- 
curied in the third decade. Males are more frequently 
affected than are females, in the proportion of 6 to 4. 

Pathology. There are four stages in the pathology 
of lobar pneumonia: 

(1) Engorgement. 

(2) Red hepatization. 

(3) Grey hepatization. 

(4) Resolution. 

1. Engorgement. The pulmonary capillaries are mark¬ 
edly congested, and some red blood-cells appear in the 
air-spaces of the lung. 

2. Red Hepatization. The affected lobe is in the pro¬ 
cess of consolidation or solidification. The air-spaces 
are more or less filled with an exudate composed of red 
blood-cells, fibrin, and some white blood-cells. The lung 
is much firmer than normal, is swollen, and pits on 
pressure. 

3. Grey Hepatization. The affected lobe is solid. If 
a piece of it be put in water, it at once sinks, showing 
that it contains no air. The lung capillaries are obliter¬ 
ated, and the exudate is most abundant, being composed 
of some red blood-cells, but chiefly of white blood-cells, 
fibrinous threads, and bits of detritus. The lobe pits 


128 


CLINICAL MEDICINE FOR NURSES. 


deeply on pressure, and is more or less of the consistency 
of liver. 

4. Resolution. This is the beginning of the stage of 
repair. The fibrin threads break up. The white blood- 



Fig. 7.—Acute lobar pneumonia. Leitz obj. No. 7, without 
ocular. The alveolar spaces are filled with leukocytes and 
fibrin. (From the collection of Dr. A. G. Nicholls. Vol. I. 
“The Principles of Pathology,” by J. George Adams, M.D.) 


cells show fatty degeneration. The lobe loses its solid 
feel, and becomes more soft and boggy. The capillaries 
again become visible, and gradually the entire exudate is 
completely absorbed, leaving 1 the lobe in its former nor¬ 
mal condition. 




LOBAR PNEUMONIA. 


129 


Symptoms. A short description of a typical attack 
of lobar pneumonia will first be given, and then the vari¬ 
ous symptoms will be taken up more in detail. 

Typical Attack. An individual in apparently perfect 
health is suddenly seized with a hard, shaking chill, 
coupled with a sharp, intense pain in the side, and high 
fever, ranging from 103° to 105°. The face is flushed, 
the eyes bright, the expression anxious, the pulse full and 
bounding, the respirations rapid, shallow and usually ac¬ 
companied by an expiratory grunt. There is cough, dry 
and hacking at first, later deeper and looser. The fever 
ranges between 102° and 105°, with slight morning re¬ 
missions, until, it terminates by crisis—that is to say, the 
fever drops several degrees within a few hours, and leaves 
the patient relatively comfortable. Herpes frequently ap¬ 
pears on the lips. There may be cyanosis, and delirium is 
common at the height of the disease, which lasts on an 
average about a week. 

Convalescence is usually fairly rapid in those that re¬ 
cover, but the mortality is high. 

Symptoms in Detail. —Onset. There are two types of 
onset: 

1. Sudden, described in the preceding paragraph. This 
is the more common mode in patients with good resisting 
powers. 

2. Gradual. This mode of onset often denotes poor 
resistance. The temperature in this case does not run as 
high. The mental symptoms, especially stupor, are more 
marked, consolidation of the lung is protracted, compli¬ 
cations are more to be feared, and mortality is higher. 
The gradual mode of onset occurs more frequently in in¬ 
dividuals past middle life. 


9 


130 


CLINICAL MEDICINE FOR NURSES. 


Pain . Caused by the inflammation of the pleura over 
the involved portion of the lung, resulting in a dry 
pleurisy. The pain is best described as lancinating, and 
is often referred to as a “stitch in the side/’ Sometimes 
when that portion of the pleura resting on the diaphragm 
is involved, the pain may be referred to the abdomen, and 
instances are on record where a diagnosis of appendicitis 
has been made. 

The pain is aggravated by talking, deep breathing, sneez¬ 
ing, coughing, and, in fact, any act that causes increased 
friction between the inflamed layers of the pleural mem¬ 
brane. 

Fever. This varies greatly. In typical cases, in pa¬ 
tients with good resisting power, it usually attains a 
maximum of from 103° to 105° at the height of the 
disease. 

In cases with poor resistance the temperature may not 
surpass 101° or 102° F. Such patients do badly, as a rule, 
circulatory failure often occurring. 

The crisis is sometimes preceded by a greater elevation 
of temperature, and occurs most frequently on the 5th, 
7th, and 9th days of the disease. 

The crisis in typical lobar pneumonia is one of the most 
striking phenomena met with in disease. A patient that 
has been running a temperature from 103° to 105°, that 
has been, cyanotic, with labored breathing, with a pulse- 
rate between 120 and 130, perhaps actively delirious, and 
obviously in every way desperately ill, will, at the end 
of from six to eighteen hours, be found with a prac¬ 
tically normal temperature, a respiration-rate but little 
above normal, the pulse-rate in proportion, all signs of 
delirium gone, a gentle perspiration taking the place of 
the raging fever, and the entire picture transformed 


LOBAR PNEUMONIA. 


13L 


from one of extreme critical illness to one of relative 
comfort and comparative safety. Moreover, on physical 
examination the lungs will be found to present almost 
identically the same signs that existed before the crisis. 
What has happened? It would appear that the general 
infection has run its course, has finished its work, and, 
having fought to its last gasp, has suddenly uncondition¬ 
ally surrendered. 



Fig. 8.—Temperature curve in typical attack of lobar 
pneumonia. 

Often, indeed, it must be noted, the occurrence of the 
crisis is marked by very serious symptoms of heart and 
respiratory failure, necessitating great watchfulness and 
vigorous stimulation; but if the patient can be safely 
tided over a few very anxious hours, the outlook is 
good. 

The Pulse. At first the pulse is full and bounding. 
Its rate is usually about 120, though it may be somewhat 
faster. As the disease progresses the pulse becomes 
smaller and weaker. Sir James Mackenzie, a great Eng¬ 
lish authority, sums up the question of the oulse in 





























132 CLINICAL MEDICINE FOR NURSES. 

lobar pneumonia so well in a single paragraph that I 
can do no better than to quote his exact words. He 
says: 

“In all cases of acute lobar pneumonia that I have met, 
when the pulse showed even an occasional irregularity 
before the crisis was reached, death supervened. I have 
not found a single exception to this rule for over ten 
years, and while extended experience may prove it fal¬ 
lacious, irregularity of the pulse in pneumonia must, at 
all events, be looked upon as a most serious symptom. 
In pneumonia, the amount of arterial tension, the rate 
of the pulse and its rhythm are each of them among 
the most important indications we possess. Within a 
few hours after a rigor the fatal termination may be 
too plainly foretold by the character of the pulse. I 
have never seen an adult with a pulse-rate over 140 
recover/’ 

This excellent summary shows how important an indi¬ 
cation is the pulse, and how fully the nurse caring for 
a patient with pneumonia must familiarize herself with 
the condition of the circulation as expressed in the pulse. 
The nurse rather than the doctor should be the first one 
to discover any abnormality or change in the pulse. 
Often and often a life will be saved by her watchfulness, 
observation, and timely warning. 

The Heart. " While the nurse will not examine the 
hearts of her pneumonia patients, and while the pulse is 
her index as to the condition of the heart itself, still she 
should know that the strain in pneumonia is thrown pri¬ 
marily on the heart, and that which is most dreaded is 
myocardial degeneration—that is, failure and exhaustion 
of the heart muscle. This weakness may arise from 
many causes. The three most commonly causing it are: 


LOBAR PNEUMONIA. 


133 


1. Toxemia. The general poison of the disease acts 
as a distinctly harmful agent upon the muscle fibres 
forming the heart. 

2. Extensive pulmonary consolidation. When two or 
three lobes of lung are solidified, the heart may have 
such difficulty in pumping the blood through the rela¬ 
tively small unconsolidated space, that it gives way under 
the strain. 

3. Hyperpyrexia. (Excessively high temperature.) 
When the temperature reaches extreme heights, over 
106°, this condition in itself exerts a degenerative effect 
upon the heart-muscle. 

Respiration. The respiration is rapid—30 to 50 per 
minute—short and shallow. There is often an expira¬ 
tory grunt. The nostrils are seen to dilate markedly 
with each inspiration. Respiration is voluntarily and in¬ 
voluntarily restricted. Owing to the pain of the asso¬ 
ciated pleurisy respiration is shallow, and therefore car¬ 
bon dioxide (C0 2 ) accumulates in the blood. This 
exerts a paralyzing effect upon the cells in the brain, 
where the respiratory centre is located, and this paralyz¬ 
ing effect still further hampers respiration. There is 
often some cyanosis, especially of the lips and finger 
tips, though in bad cases the entire face may take on a 
dusky hue. 

Cough. Cough is an almost constant symptom in 
pneumonia. Jiirgensen says: “It is rarely useful, always 
troublesome, sometimes dangerous.” The cough is at 
first hard, dry, hacking, and paroxysmal. It is ex¬ 
quisitely painful, owing to pleurisy. Later it becomes 
looser, and abundant sputum is raised. 

Sputum. The sputum at first is very characteristic of 
pneumonia. It is tinged with blood, this tinge giving 


134 


CLINICAL MEDICINE FOR NURSES. 


it a color best described as “rusty.” It is extremely vis¬ 
cid and tenacious. The' cup or glass into which it is 
expectorated can be turned upside down without the 
sputum being spilled. I have known the sputum to be so 
tenacious that it had to be wiped out of the patient’s 
mouth and actually pulled off the tongue. As the disease 
progresses, and especially when the stage of resolution 
is reached, the sputum becomes less viscid, far more 
abundant, and often of a greenish color. 

Herpes. This consists in the appearance on the lips 
and at the angles of the mouth of vesicles which dry up, 
leaving reddish-brown scabs. Herpes, while most com¬ 
mon on the lips, may occur anywhere. Its presence is 
considered by some to be a favorable sign. 

Urine. The main feature of the urine in pneumonia 
is a decrease in the chloride content, due to the large 
amount of chlorides contained in the exudate in the lungs. 
Save for this fact, the urine presents the usual character¬ 
istics found in most acute febrile diseases. 

Bowels. There is usually constipation, though the 
bowels present nothing characteristic. In bad cases, 
there may be marked tympanites, which may prove dan¬ 
gerous by exerting upward pressure on the heart. 

Blood. An increase in the white blood-cells is the rule 
(leukocytosis). The white blood-cells in pneumonia usu¬ 
ally number from 15,000 to 50,000 (4000 to 7000 being 
the normal number). Leukocytosis is an important sign 
from the standpoint of diagnosis and prognosis. Pa¬ 
tients with little or no leukocytosis almost always do 
badly. 

Duration of Disease. Two days to three weeks; usu¬ 
ally about ten days. The longer cases must be con¬ 
sidered as suspicious. Complications may have set in. 


LOBAR PNEUMONIA. 


135 


Complications: 

1. Pleurisy. 

(a) Dry. Practically a part of the disease. 

(b) With effusion. Develops in about 6 per 

cent, of the cases. 

2. Empyema. Occurs in 2 per cent, to 5 per cent. 

of the cases. 

3. Abscess and gangrene of the lung. These are 

rare. 

4. Endocarditis. 

( a ) Simple. Fairly common. 

(&) Malignant. 

5. Pericarditis. 

6. Acute nephritis. Not uncommon. 

In alcoholic patients the mental and nervous symp¬ 
toms predominate, delirium is violent and protracted, and 
the mortality is very high. 

Prognosis. Always grave. Depends upon the fol¬ 
lowing factors: Course of temperature, pulse, and 
respiration; age of the patient, pneumonia being most 
fatal at extremes of life; alcoholism, or its absence; 
altitude, pneumonia being more fatal at high altitudes 
than at low ones; the amount of lung involvement, and 
the occurrence of complications. According to Wells, 
the mortality in 465,400 cases was 94,826, or 20.4 per 
cent. 

Treatment. We have at our command no specific 
for the treatment of lobar pneumonia. As we cannot, 
therefore, treat the disease, we must devote all of our 
efforts to treating the patient. The objects of treatment 
are threefold: 


136 


CLINICAL MEDICINE FOR NURSES. 


1. To facilitate the body’s efforts in its own behalf, 
by means of: 

( a ) Rest. 

(b) Hygiene. 

(c) Diet. 

2. To reinforce nature’s proceedings along her own 
lines. 

3. To support such organs as show signs of failing. 

Every physician in treating pneumonia has, in all 

probability, a method that he prefers to all others, and the 
nurse will, of course, faithfully carry out his orders to 
the letter. The following suggestions for treatment are 
based on broad general principles, and, taken collec¬ 
tively, will be used in practically every case. 

1. The patient must always be at rest in bed in the re¬ 
cumbent position, and the use of bed-pan and bed-urinal 
insisted upon. 

2. Fresh Air. A patient with a serious infection and 
with markedly diminished breathing space obviously 
requires all the fresh air obtainable. In many hospitals 
pneumonia patients are being kept out of doors, with 
very gratifying results, both as regards the comfort of 
the patients and the percentage of mortality. In private 
homes this mode of treatment is seldom practicable. The 
room should be airy, and the windows kept open. This 
will necessitate added vigilance on the part of the nurse,' 
in order not to allow the patient to become uncovered. 
Windows and doors should, of course, be closed in cold 
weather during the bath, the use of the bed-pan, ex¬ 
amination, or any procedure involving exposure of the 
patient. 

3. Care of the Mouth, Tongue, and Teeth. Tooth¬ 
picks with cotton on the end, which are soaked in 2 per 


LOBAR PNEUMONIA. 


137 


cent, boric acid, are good for cleaning the teeth. A 
whalebone is an excellent instrument for scraping and 
cleaning the tongue; and sweet oil, cold cream, cocoa 
butter, or vaseline are welcome applications to lips ex¬ 
coriated and raw from herpes. 

The condition of the mouth is a very good indication 
of the general care a patient is getting. The nurse that 
allows her patient's mouth to get in a foul condition is 
probably slighting that patient in other directions. 

4. Diet. The diet should be liquid or semi-solid; 
small amounts frequently administered. If the patient 
is able to take semi-solid food, many physicians believe 
in giving it. The main articles of diet are chosen from 
the following list: milk, oatmeal, rice, hominy, eggs, 
cup custard, ice cream, broths, gelatine, jellies, and the 
various substitutes for milk. 

Sufficient water should be given to slake the thirst. 
If the patient shows signs of becoming stuporous, it is 
well to force the amount of water. 

5. Bowels. An initial purge with calomel, followed 
by a saline, is usually given. Later, the bowels are 
moved by enemata, though some physicians prefer laxa¬ 
tives by mouth. 

6. Fever. High fever, save when accompanied by 
delirium or marked signs of toxemia, is generally not in¬ 
terfered with. With very high temperatures—106° or 
over—cold packs and sponges are resorted to. At the 
present time the majority of physicians do not look with 
favor upon the administration of drugs to reduce the 
fever of pneumonia patients. 

7. Cough. When due to pleurisy, heat or cold, mus¬ 
tard, iodine, or strapping with adhesive plaster over the 
painful area will often help. Strapping has the disad- 


138 CLINICAL MEDICINE FOR NURSES. 

vantage that it interferes with subsequent chest exami¬ 
nations. Often, drugs, such as codeine, heroin, or even 
morphia must be resorted to. 

The productive cough that brings up sputum is, on . the 
whole, beneficial, and is usually not treated. If very ex¬ 
hausting, steam inhalations will often be of aid. Some 
expectorant mixture is often prescribed. 

8. Toxemia. Usually best combated by forcing the 
patient to drink as much water as possible, and by in¬ 
jecting salt solution under the skin (hypodermoclysis), 
or by introducing salt solution into the bowel and allow¬ 
ing it to become absorbed (enteroclysis). The method 
known as the “Murphy Drip” is excellent for this purpose. 

9. Delirium. This is helped by the methods mentioned 
in the preceding paragraph. The most efficient and most 
used drug for this condition is morphia, as in addition 
to quieting the patient it causes restful sleep. 

10. Circulatory System. This must be most carefully 
watched by the nurse, and the slightest danger sign com¬ 
municated to the physician. 

Many physicians (the author among them) believe in 
full digitalization of the heart at the beginning of every 
case of lobar pneumonia. The arguments in favor of 
this plan of treatment are two-fold: 

1. Full digitalization of the heart does no harm. 

2. Fully 10 per cent, of the cases of lobar pneumonia 
develop auricular fibrillation (Cohn) in which digitali¬ 
zation produces its most brilliant results. The method of 
digitalizing the heart in lobar pneumonia differs in no 
way from that described in connection with full digitali¬ 
zation in heart-failure ( q.v .). 

In addition to the use of digitalis, excellent results are 
obtained from the rational administration of morphia. 


LOBAR PNEUMONIA, 


139 


Rest is badly needed. Rest from the disturbing dyspnea, 
rest from the racking cough, both of which (dyspnea and 
cough) entail muscular exertion, thus throwing more 
strain on the heart muscle. The precise dose of morphia 
cannot here be given or even suggested. The principle 
of its administration is merely set forth. It is an unques¬ 
tionable fact that many cases of lobar pneumonia can be 
satisfactorily managed with the following armamentarium: 

1. A good nurse. 

2. An active tincture of digitalis. 

3. A variable amount of morphia. 

4. Some good laxative. 

5. An observing and careful physician. 

In severe cases, in full-blooded individuals with marked 
labored breathing and cyanosis, bleeding from a vein to 
the amount of 12 to 16 ounces is often of great help. 

11. Specific Treatment. It has been found by Cole and 
his associates at the Rockefeller Institute that the pneu¬ 
mococci present in the sputum of pneumonia patients can 
be divided into types which have been designated I, II, 
III, IV. In any given case sputum is taken to the labora¬ 
tory, and the type to which the pneumococci belong is 
determined. An immunizing serum corresponding to the 
particular type is then administered. Good results have 
been obtained from this method of treatment in cases 
showing pneumococci of type I. 

12. Collapse. Collapse in pneumonia may occur at any 
time. Its onset is sudden, and the likelihood of its oc¬ 
currence increases as the time of the crisis approaches. 
The main symptoms are: 

Rapid prostration. 

Chilly sensations. 

Ashen face. 


140 


CLINICAL MEDICINE FOR NURSES. 


Cold, clammy skin. 

Restlessness and air-hunger. 

Rapid, shallow, gasping respiration. 

Soft, compressible, often almost imperceptible pulse. 

The condition is a most urgent one, and prompt action 
is necessary. The nurse may not be able to get the doc¬ 
tor at once, and her patient may die while she is calling 
up various numbers on the phone, trying to locate the 
physician. She must act on her own initiative. The fol¬ 
lowing plan is set forth in the belief that it will meet 
with no opposition from any physician: 

Apply heat to the extremities in the shape of hot 
cloths, hot bottles and hot-water bags. 

Give diffusible cardiac and respiratory stimulants: 

Strong ammonia on towel held near patient’s nose; 

Aromatic spirits of ammonia, 1 teaspoonful in water; 

Camphor in oil, 9 to 15 grains hypodermically; 

Adrenalin chloride, 1: 1000 solution, 20 minims 
hypodermically; 

Ether, 15 to 20 drops hypodermically; 

Whiskey, 15 to 20 drops hypodermically. 

The nurse should not be satisfied with giving any one 
of these alone. It will not be necessary to give them all, 
but two, three or four should be given, as in such a crisis 
the heart seems to react better from the effects of a 
“broadside” than from “single shots.” It seems useless 
to add that the physician should be summoned at once, 
the nurse getting some person to trace him unceasingly 
until he is found. 

13. Convalescence. It is quite impossible to give any 
absolute rules for the management of convalescence, for 
each case is a law unto itself. Convalescence, in uncom- 


LOBAR PNEUMONIA. 


141 


plicated pneumonia is relatively rapid. Care must be ex¬ 
ercised when the patient first sits up in bed, and on no 
account must he be allowed suddenly to raise himself, as 
several cases of sudden death from the unexpected strain 
on the heart are on record, as the result of such an in¬ 
discretion. Progress must he slowly made, and vigilance 
must never be relaxed until the nurse is dismissed from 
the case. 


CHAPTER XIX. 

BRONCHOPNEUMONIA. 

Bronchopneumonia is perhaps not so much a dis¬ 
ease as a condition or lesion, and follows no set rules, 
either as to its causation or symptoms. It attacks pref¬ 
erably those at the extremes of life: infants, young 
children, and old persons save when complicating influ¬ 
enza, when no age is exempt. It rarely occurs as a pri¬ 
mary disease, but usually as a sequel of a pre-existing 
bronchitis, and is particularly frequent as a complica¬ 
tion of various diseases, especially influenza and the acute 
eruptive fevers of. childhood, such as measles. Broncho¬ 
pneumonia frequently occurs after or during whooping- 
cough. 

No specific organism is the causative factor in bron¬ 
chopneumonia, though the disease is invariably of germ 
origin. The pneumococcus, the staphylococcus and the 
influenza bacillus are all found, the pneumococcus being 
present most frequently. 

The pneumonic area, or area of consolidation, occurs 
in small patches, surrounding a bronchus, which is found 
filled with gray mucus, while the surrounding air-vesicles 
are filled with an exudate somewhat like that found in 
lobar pneumonia. 

Symptoms. 

1. In Children. Following a bronchitis, with its slight 
temperature, cough and expectoration (if the child is 
not too young to raise anything), bronchopneumonia sets 
in with increase in all these symptoms. The child be¬ 
comes restless, and cough and dyspnea become more 
marked. Respiration is short, shallow, and may range 
from 50 to 75 per minute. Cyanosis may be present; 
(142) 


BRONCHOPNEUMONIA. 


143 


The nostrils dilate with every inspiration, and the child 
is seen to strain to get its breath. Temperature varies 
greatly, usually reaching 103°, though it may rise as 



Fig. 9.—Bronchopneumonia. A, normal lung tissue; B, 
small bronchus surrounded by consolidated lung tissue; C, 
thickened wall of bronchus; D, blood-vessels; E, small 
bronchus. (“Infancy and Childhood,” Holt.) 

high as 105°, and may reach 108° before death. The 
fever curve is irregular, but constantly above normal. 
The pulse is always rapid, often reaching 140 beats per 
minute. Sometimes it is so fast that it cannot be 




144 


CLINICAL MEDICINE FOR NURSES. 


counted. Vomiting and diarrhea are frequent. The 
temperature falls gradually, the entire duration of the 
disease being from two to three weeks. The child may 
improve, and then, with the formation of fresh pneu¬ 
monic patches, all the symptoms may return with their 
former or with increased severity. 

2. In the Aged. In old people there are frequently no 
definite symptoms, and the signs of bronchopneumonia 
are discovered by the physician during a routine exami¬ 
nation of the lungs. Cough and sputum may be slight 
or absent, a low grade of temperature (100° to 101°) 
may or may not be present, and the main symptoms noted 
may be an increase in dyspnea on very slight exertion, 
and a gradual failure in strength. So many of these 
cases occur in elderly persons suffering from a chronic 
bronchitis of long standing, that the development of a 
bronchopneumonia is thought to- be merely a flare-up of 
the bronchitis. The disease is very apt to attack persons 
that are bed-ridden from other causes, whose hearts are 
so weak that the blood is not propelled through the lungs 
with proper velocity, and who lie for days and weeks in 
almost the same position. 

Prognosis. This depends largely on two factors: 

1. Age. The younger the child the greater the mor¬ 
tality; the older the patient the greater the mortality. 
Probably from 30 to 50 per cent, of all cases occurring 
in childhood terminate fatally. 

2. The primary diseases of which bronchopneumonia 
is a complication. These are too numerous to be dis¬ 
cussed in detail. 

Treatment. The treatment of bronchopneumonia is 
hygienic and symptomatic. Some authorities are loud in 
their praises of out-of-door treatment, such as is used in 


BRONCHOPNEUMONIA. 


145 


tuberculosis and in hospital practice in lobar pneumonia, 
In summer this is unquestionably indicated; but in win¬ 
ter, as many patients with bronchopneumonia are run 
down and debilitated, care and caution must be exer¬ 
cised. Most physicians prefer a rather warm room, 65° 
to 70 , if necessary the air being kept moist with steam. 

La Fetra says: “Cold air is particularly indicated in 
cases with little bronchitis and during convalescence; 
while during the acute congestive stages of pulmonary 
infection, with considerable bronchitis, warm and moist 
air is preferable.” 

Flannel is usually worn next to the skin. Moderately 
high fever usually needs no interference; but when signs 
of toxemia are present, such as restlessness, headache 
and delirium, the temperature must be artificially low¬ 
ered. Water in some form is the usual method, as, 
especially in young children, antipyretics are not con¬ 
sidered advisable. Cold sponges, wet packs and cold 
compresses over the chest (Priesnitz applications) are 
relied upon. The latter are made by wrapping the chest 
with one layer of flannel that has been wrung out of 
water at room temperature, and covering this with three 
or four layers of dry flannel. This form of hydrotherapy 
is efficient in lessening nervous symptoms, and also to a 
lesser extent in lowering fever. Cyanosis must be met 
by stimulation of the heart if that organ is weak, and by 
trying to divert the blood to the surface of the body. 
For this purpose a mustard poultice applied to chest and 
back is good, but the nurse must be very careful not to 
leave this on too long, as it may greatly irritate the skin 
of a young child. The flannel applications to the chest, 
above referred to, are often of service. Older children 
should have their position frequently changed, and 
10 


146 


CLINICAL MEDICINE FOR NURSES. 


babies should be taken up and carried about from time 
to time. For bad and persistent cyanosis, oxygen inhala¬ 
tions are of value. 

The heart often needs stimulation. Alcohol, now 
so frowned upon generally in medicine, is still conceded 
a place in the treatment of heart failure in broncho¬ 
pneumonia. Brandy is the favorite form in which it is 
given. Other stimulation varies in no way from that 
given for heart-failure in other acute diseases. Food 
should be liquid or semi-solid, depending upon the age 
of the child. 

Cough and pain, that call so insistently for treatment 
in lobar pneumonia, rarely require special measures in 
bronchopneumonia. If very distressing, codeine is 
effectual, though in young children the use of opiates in 
any form is usually avoided as long as possible. 

Convalescence must be guarded, as these patients are 
prone to relapse. 

The treatment of bronchopneumonia in the aged pre¬ 
sents no distinctive features. Stimulation must fre¬ 
quently be resorted to, and the problem is mainly that of 
building up the patient’s strength and trying to overcome 
the primary disease of which bronchopneumonia is a 
complication. Particular attention must be given to 
changing the position of the patient frequently to pre¬ 
vent hypostatic congestion. In the aged, alcohol seems 
to have a particularly beneficial effect in keeping up the 
strength and in enabling the debilitated individual to 
fight the infection. 


CHAPTER XX. 


INFLUENZA. 

Influenza is an acute infectious disease affecting the 
entire body and characterized by symptoms of a catarrhal 
inflammation of the upper respiratory tract, by general 
aching, and by a prostration out of all proportion to the 
other evidences of disease. It was believed to be caused 
by the influenza bacillus of Pfeiffer (discovered in 1893) 
but exhaustive bacteriological investigations during and 
subsequent to the pandemic of 1918-19 have failed to 
establish this organism as the one and only cause of 
influenza. In connection with the pandemic of 1889- 
1890 it is interesting to read a quotation from Dr. F. T. 
Lord, of Boston, showing the spread of the disease and 
how relatively accurately it paralleled that of human 
travel. 

“The origin of this pandemic (1889-90), like many 
others, is uncertain. The outbreak in Hongkong in the 
fall of 1888, in Buckara in the middle of May, 1889, or 
in Tomsk in the beginning of October, may have been 
the starting point of the epidemic which occurred in St. 
Petersburg (now Petrograd) toward the end of October. 
By November the disease had swept through Germany 
and France; by December through Austria, Sweden, 
Denmark, Switzerland, Italy, Spain, Portugal, Belgium 
and the Netherlands, England, the Balkan States, and 
North America. By March it had reached India and 
Australia; by April and May, China and the Gold Coast 
of West Africa. Berlin was invaded the middle of 

(147) 


148 


CLINICAL MEDICINE FOR NURSES. 


November; Paris from the 17th to the 20th of Novem¬ 
ber ; London the second week of December; Boston and 
New York the 17th of December. Within a year it had 
visited nearly all parts of the world.” 

The great mass of evidence is in favor of the direct 
transfer of the disease from person to person. The pan¬ 
demic of 1918 is supposed to have had its origin in Spain, 
hence the nickname it received of “Spanish Influenza.” 
Its ravages among the civilian and military population of 
this country and among the nations of Europe are, of 
course, well known to all. The essential cause of influ¬ 
enza is as yet unsettled. Pfeiffer’s bacillus plays a role 
and an important one in its causation, being found in a 
relatively large percentage of all cases, but other organ¬ 
isms, notably the streptococcus and the pneumococcus can¬ 
not be ignored. It is the general consensus of opinion to¬ 
day that no one organism is responsible for the existence 
of influenza in the same sense that the tubercle bacillus 
is the cause of tuberculosis or the diphtheria bacillus the 
cause of diphtheria, but that to several organisms acting 
together must be ascribed the occurrence of this disease. 
One particular strain of streptococcus deserves special 
mention, the S. hemolyticus, (deriving its name from its 
ability to hemolyze.or bring into solution red blood' cells) 
which was present in the vast majority of fatal cases. 

Symptoms. 

Onset. This is usually sudden and sometimes strikingly 
so, many cases being on record where a man has left his 
office feeling comparatively well, and on the way home has 
practically collapsed and has had to wait for assistance in 
order to enable him to get to his destination. 

The disease develops rapidly, within a few hours, and 
the patient is seen to be profoundly ill. The fever is high 


INFLUENZA. 


149 


(102 to 104°), the pulse over 100, there is headache and 
intense aching of practically every portion of the body. 
The aching is described as intense, agonizing, unbearable. 
It seems to be situated in the deeper portions of the body, 
the bones, the joints, the back. The painful areas are, 
however, not tender to pressure, showing that there is no 
local inflammation but that the pain is due to a general 
toxemia. In addition there is profound depression, not 
only mental but also physical. The victim is too sick to 
care “whether school keeps or not” and lies in bed prac¬ 
tically oblivious to his surroundings. It is due to this 
depression that such distressing scenes were beheld during 
the epidemic of 1918 when entire families were attacked 
almost simultaneously and practically lay in their tracks, 
unable to do anything. Parents and children languished 
in bed, incapacitated, caring nothing as to whether food 
were to be had or whether the ordinary rules of hygiene 
and detent living were adhered to. They became for the 
time merely individual masses of suffering, toxic bundles 
of human flesh, helpless and hopeless! 

In uncomplicated cases the disease runs its course in 
from four to seven days, the fever subsides by lysis and 
convalescence ensues, the prostration and physical weak¬ 
ness being protracted so that, to quote Dr. Charles L. 
Minor, of Asheville, “the characteristic picture of influ¬ 
enza is that you feel sick so long after you are well.” 

Influenza is characterized by a catarrhal inflammation 
of the entire upper respiratory tract, there being conjunc¬ 
tivitis, rhinitis, pharyngitis, tracheitis, and bronchitis. 
There is cough, at first harsh and unproductive, accom¬ 
panied by a burning pain under the sternum, the cough 
becoming gradually looser and bringing up sputum. 
Rarely cases are seen in which the entire body is, as it 


150 


CLINICAL MEDICINE FOR NURSES. 


were, overcome by an intense toxemia. The skin takes on 
a dusky hue, the face is grey and pinched, there is dysp¬ 
nea, the pulse is weak and rapid, and death ensues within 
twenty-four to seventy-two hours; apparently from an 
overwhelming systemic poisoning. Save in this type of 
case influenza is almost never fatal except as a result of 
complications. 

Complications. 

Bronchopneumonia. This is by all odds the most fre¬ 
quent and also the most severe complication of influenza. 
'It appears in certainly 20 per cent, of the cases. It may 
set in within twenty-four hours of the onset or when the 
patient is believed to be practically convalescent. In the 
former case its presence is discovered on physical exam¬ 
ination. In the latter case by an increase in temperature, 
pulse, and respiration rates, the latter being particularly 
important. The pneumonic area begins usually in the 
lower lobes of the lungs. There may be one area or 
several on one or on both sides. These areas may coal¬ 
esce, thus giving a picture resembling true lobar pneu¬ 
monia. As one area clears up another area may become 
involved. 

Otitis Media. This condition is frequent but does not 
differ in its symptoms nor in its treatment from its occur¬ 
rence when complicating any other disease. 

Meningitis. Not frequent. Presents the usual symp¬ 
toms of meningitis from any cause. 

Sinus Involvement. Both frontal and ethmoidal sinuses 
may be the seat of a catarrhal or suppurative process 
requiring exploration and drainage. Pleurisy with ef¬ 
fusion and empyema are met with, usually as complica- 
cations of pneumonia and requiring no special mention 
here as to their management and treatment. 


INFLUENZA. 


151 


In short, we find in bronchopneumonia, otitis media, 
and the involvement of the accessory sinuses of the nose 
the main complications of influenza. 

Prognosis. This depends upon : 

(a) Presence, absence, or stage of an epidemic. It is 
well known that the virulence of the infecting agent in¬ 
creases in an epidemic until a “peak” is reached and then 
diminishes. The prognosis will be largely dependent upon 
the stage in the epidemic at which a given case occurs. 

( b ) Complications. Bronchopneumonia renders the 
(prognosis usually more grave. There will be a mortality 
of from 10 to 30 per cent, in the pneumonia cases. 

( c ) Treatment. The author has no idea of suggesting 
a “treatment” for influenza for he is absolutely skeptical 
as to the efficacy of any plan followed. He is convinced, 
however, that the care that can be given the patient is of 
vital importance. If, on becoming ill, an individual can 
at once go to bed, resort to absolute rest, be kept warm 
and comfortable, and have the intelligent services of a 
good, nurse, his chances of recovery are excellent. If, 
on the other hand, he must keep going as long as possible, 
must then wait on himself, get up to secure food and to 
go to the toilet, try to keep the little fire going in the grate, 
and go to the kitchen cupboard to get the tickets for the 
milkman, such an individual runs more chances of com¬ 
plications setting in, and, therefore, his prognosis is not 
as good. Nursing care plays a more important part in the 
management of influenza than any other factor and if the 
choice must rest between a good nurse and a good doctor 
choose the former! 


152 


CLINICAL MEDICINE FOR NURSES. 


Treatment. 

There is no treatment for influenza as such. So-called 
treatment consists in the management of the individual 
who has influenza. Treatment must be subdivided into: 

(a) Prophylactic. 

( b ) Active. 

(a) Prophylactic treatment. The author confesses to 
a marked skepticism as to the efficacy of the various 
methods of prophylactic treatment employed save one: 

Avoidance of Crowds. This is of paramount import¬ 
ance. We do not know how the infection of influenza is 
communicated, but it has been absolutely proven that 
the incidence of cases of influenza increases after 
public gatherings. The best proof of this is to be 
found in the tables compiled by the Boards of Health 
of countless cities in this country and abroad in the fall of 
1918. The peak of the epidemic was adjudged to be in 
October. The number of cases began to decline. Then 
came November 11th and the Armistice, celebrated almost 
throughout the world by public gatherings. Immediately 
thereafter the number of cases of influenza markedly in¬ 
creased. 

In the presence of the possibility of an epidemic, 
schools, theatres, movies, cafeterias, department stores, 
and churches should be closed. Street cars should 
be forced to have half their windows open and congre- * 
gations of individuals in any building and even in the 
open air should be discouraged. Ventilation should be 
particularly free in all dwellings. Social gatherings should 
be prohibited. Individuals should give particular care to 
the hygiene of their bodies, particularly of the nose and 
mouth. Persons coughing or sneezing should invariably 
cover the mouth and nose when indulging in such acts. 


INFLUENZA. 


153 


It has been claimed that infection was conveyed through 
nasal and pulmonary secretions but this has been largely 
disproved by the failure of individuals who had heroically 
allowed their noses and mouths to be sprayed with the 
nasal secretions from influenza patients to contract the dis¬ 
ease. Hence the wearing of gauze masks, though psychi¬ 
cally advisable, probably plays a small part in prophylaxis. 
When all is said and done, the question resolves itself into 
one of the relative strengths of individual resistance and 
invading virus as evidenced by the fact that many persons 
taking no precautions are not attacked, while many others, 
taking every possible care, fall victims to the disease. To 
emphasize again, the main elements in prophylaxis are: 

1. The avoidance of crowds. 

2. Personal hygiene and cleanliness. 

( b ) Active Treatment. There being no treatment for 
influenza, one’s efforts must be confined to the treatment 
of the individual who has influenza. This is simple and 
conducted along general lines. Most important is bed rest. 
Were every individual the victim of influenza to go to bed 
and stay there two weeks the incidence of complications 
and hence of mortality would be enormously lessened. 
Bed rest is essential and should be complete and persisted 
in until the temperature has been normal for at least five 
days and until there is cessation of cough and sputum. 
An initial purge with castor oil or calomel is indicated. 
Acetylsalicylic acid (aspirin) in 5-grain doses every 
three or four hours is good. An opium suppository will 
often relieve the intense aching in the back. Mustard to 
the chest, front and back, is advisable and codeine to 
control the cough. Some expectorant such as Brown mix¬ 
ture is of service. Food should not be withheld and full 
diet is desirable as soon as the appetite of the patient 


154 


CLINICAL MEDICINE FOR NURSES. 


will permit. The drinking of large quantities of water is 
essential and the greater the total daily fluid intake the 
better the outlook. Bromides and frequently morphia are 
advisable in the acute stage of illness. Several hours of 
quiet sleep should be secured nightly if possible. Bodily 
warmth and comfort are of paramount importance. The 
earnest and conscientious nurse will help more in a case 
of influenza than the best doctor in the world. The pa¬ 
tient must not be allowed to get up and try to go about 
too soon, as it must be remembered that influenzal and 
post-influenzal prostration is marked, and that complica¬ 
tions serious and dangerous may set in when the patient 
is apparently on the high road to recovery. 

Treatment of Complications. Pneumonia, otitis media, 
etc., require no special mention here, as their treatment 
is similar to that when they are met with as complications 
of other conditions. 


CHAPTER XXL 
TYPHOID FEVER. 

Typhoid fever is essentially a general infection with 
the typhoid bacillus, manifesting itself by a continued 
fever, a skin eruption, and intestinal ulceration of 
greater or less severity. The fever runs an average 
course of from three to four weeks, and terminates by 
lysis, i.e., gradual descent. Typhoid fever presents 
greater variations in its manifestations than any other 
acute infectious disease, and may be complicated by 
conditions affecting practically every organ in the body. 
In no disease is careful nursing, conscientious observation, 
painstaking attention and correct interpretation of changes 
more necessary and valuable than in typhoid fever. The 
nurse that has had extended experience in the care of this 
disease alone, should be well qualified to assume responsi¬ 
bility in the vast majority of medical cases. 

HISTORY. 

In the writings of Hippocrates, Galen and others of 
the ancients, it is not possible to distinguish typhoid as 
an entity. Typhus and typhoid, the plague and, perhaps, 
malaria and relapsing fever, were apparently grouped to¬ 
gether. The greatest difficulty seems to have lain in the 
separation of typhoid and typhus fevers. 

It would be wearisome to give a list of all those quoted 
in the history of this varied disease, but somewhat de¬ 
tailed mention must be made of Willis, who described an 
epidemic occurring in 1643 which leaves no room for 

(155) 


156 


CLINICAL MEDICINE FOR NURSES. 


doubt as to its identity with typhoid fever: “Among the 
features he describes were headache, nosebleed, delirium, 
an eruption like flea-bites, diarrhea, abdominal disten¬ 
sion, intestinal hemorrhage, incontinence of urine and 
feces, emaciation in prolonged attacks, the long course 
and the slow recovery without crisis, or the gradual 
progress to a fatal issue.” 

“In the history of one patient he describes what was 
probably an instance of death from perforation: Tains 
and torments cruelly infected his belly, that crying out 
and moaning night and day, he sent forth his most 
heavy complaints; his hypochondria and abdomen were 
tumid like a tympany, and mightily distended.’ 

Willis made the observation that the contagion of this 
disease was slow, but that gradually a household or a 
community might be infected, and mentions that some of 
those nursing the patients contracted the disease after 
a time. He appears to have clearly separated typhoid 
fever from the plague and typhus fever, and to have 
appreciated in a remarkable way many of the clinical 
manifestations as well as the features of epidemics. 

Among those following Willis that wrote of diseases 
that were probably typhoid should be mentioned Syden¬ 
ham, Baglivi, Hoffman in Halle in 1699, and again in 
1728, Huxham of Plymouth, who in 1737 “had taken 
notice of the very great difference there is between the 
putrid, malignant (typhus) and the slow, nervous (ty¬ 
phoid) fever.” Riedel in Germany wrote in 1748 of 
typhoid under the name of Darmfieber (intestinal fever) ; 
and Roderer and Wagler studied an epidemic in Gottin¬ 
gen (1757 to 1762) which must have been one of typhoid. 

More modern descriptions of the disease date from 
1813 to 1850, and claim France and our own United 


TYPHOID FEVER. 


157 


States as the countries of their origin. In 1813 Petit and 
Serres described “entero-mesenteric” fever. It is worthy 
of note that in 1824 our countryman, Nathan Smith, pub¬ 
lished a description of typhoid fever. He did not dis¬ 
tinguish between typhoid and tyhus, for he evidently 
saw only one of the two diseases, but his description 
stands as one of the classics of American medicine, and 
is one of the best early accounts of the disease. 

In 1829 Louis’ great work appeared in which the 
name “typhoid” was first used. At this period typhoid 
alone prevailed in Paris, and it was universally believed 
to be identical with the continued fever of Great Britain, 
where, in reality, typhoid and typhus coexisted. The in¬ 
testinal lesion was at that time regarded as an acciden¬ 
tal occurrence in the course of an ordinary typhoid. 
Louis’ students, returning to their homes in various 
countries, studied the disease thoroughly. One of them, 
Gerhard, of Philadelphia, recognized the prevalence at 
home of the same disease that he had studied with 
Louis in Paris, and to him, by the publication of his 
articles in the “American Journal of the Medical Sci¬ 
ences” in 1835 and 1839, is due the great honor of having 
first clearly laid down the differences between typhoid 
and typhus fevers, and of having established a separate 
individuality for the former. 

Almost simultaneously (1833) James Jackson, Jr., of 
Boston, demonstrated in his father’s wards at the Massa¬ 
chusetts General Hospital the identity of the so-called 
typhus of this country with the typhoid of Louis. In 
1838 and 1839 James Jackson, Sr., and Enoch Hale pub¬ 
lished articles which, together with Gerhard’s contribu¬ 
tions, served to make typhoid well known in the United 
States before it was recognized abroad as a clinical and 


158 


CLINICAL MEDICINE FOR NURSES. 


pathological entity. Shortly thereafter, the studies of 
Griesinger in Germany, and of Murchison and Tenner in 
England, did much to spread knowledge of the. disease. 

Two additional facts are of historical importance. 
The first of these is, that clear views on the modes 
of infection were first published by Budd, of Bristol, 
in the London “Lancet,” 1856-1860. He believed that 
the infective agent was to be found in the stools of the 
typhoid patient, and that the disease never arose spon¬ 
taneously, but always from a specific source. He held 
that a previous focus was necessary before a neighbor¬ 
hood could be infected, and by the study of many epi¬ 
demics recognized the result of the introduction of infec¬ 
tion into a community, and noticed that a few strag¬ 
gling cases might later be followed by a larger outbreak. 
He considered that an exceedingly small amount of in¬ 
fective material was able to convey the disease, and, 
arguing from this belief, he put forward the view that 
the possibility of infection could be prevented if the stools 
were thoroughly disinfected. His views are essentially 
correct; and Budd may be regarded as the first to recog¬ 
nize the leading points in the transmission of the disease. 
The second point to be mentioned is the discovery of the 
specific germ causing the disease—the typhoid bacillus, 
or Bacillus typhosus, by Eberth, in 1880. 

“Typhoid fever occurs in the tropics, and at far 
northern and southern latitudes, at sea-level and in the 
mountains, in the city and in the country, and practically 
everywhere man may go, and local conditions do not 
prevent the dissemination of the disease. The Bacillus 
typhosus has about the same limits of latitude and longi¬ 
tude as man himself, and no country or race is known to 
be immune from the disease.” 


TYPHOID FEVER. 


159 


Schuder, in a study of 638 epidemics from 1870 to 1899, 
found the infection to be carried by water in 71 per cent. 
In Hamburg from 1885 to 1888 there were 15,804 cases 
of typhoid fever. The water supply at that time was ob¬ 
tained from the Elbe, not far from where the sewers dis¬ 
charged. The neighboring city of Wandsbeck, with a 
different water supply, was practically free from the dis¬ 
ease. In Paris, as a result of a better water supply, the 
death-rate from 1882 to 1902 due to typhoid fever was 
reduced from 142 to 17 per 100,000 population. 

These few figures show the paramount role played by 
water in carrying infection. The brief historical sum¬ 
mary is interesting as setting forth the early gropings 
for a clue to this universal scourge, and as showing the 
effect of the breaking forth of the light of knowledge and 
the gradual comprehension of the value of a strict 
prophylaxis in limiting the ravages of a disease that even 
now exacts a yearly toll of over 25,000 lives in the 
United States alone, and that is wholly and completely 
preventable. 

Etiology. The essential cause of typhoid fever is 
the typhoid bacillus, and that alone. This bacillus is 
motile, flagellated (possessing hair-like processes), grows 
£>est in bouillon or milk, is very resistant to cold, being 
able to live for three months in ice, is usually killed by 
a temperature of 60° C. (140° F.), is always present in 
the stools, and usually in the urine. 

Modes of infection: 

1. Direct. By contact with the stools or urine con¬ 
taining typhoid bacilli. The hands becoming contami¬ 
nated, bacilli are easily taken into the mouth, and so into 
the intestinal canal. Carelessness with bedclothes, bed- 
pans, urinals, or any articles or utensils coming in con- 


160 CLINICAL MEDICINE FOR NURSES. 


tact with the excreta of the patient may very easily 
cause attendants to acquire the disease. 

2. Water. This is by far the most common source of 
all typhoid epidemics. If the water supply of a com¬ 
munity is infected, practically every one not immune to 
the disease is taken ill. Carelessness in disinfection and 
disposal of excreta, or an inadequately protected water¬ 
shed, pave the way for an infected water supply. The 
accompanying diagram illustrates schematically how a 
water supply may become infected. 



Fig. 10.—Diagram to illustrate water supply of town. 1, 
town; 2, water reservoir; 3, house with typhoid patient—no 
care taken to disinfect stools; 4, spot where stools and urine 
are emptied; 5, arrows showing hillside down which bacilli 
are washed by rain, until infected rain-water reaches reser¬ 
voir which in turn becomes polluted; 6, pipe running from 
reservoir to town. 

While the diagram shows how the water supply to a 
whole town may become infected, there are many other 
ways in which water may indirectly prove to be the 
channel of infection. Some of these will be briefly men¬ 
tioned. 

3. Food: 

(a) Milk. Often contaminated through infected 
water used to wash the cans, or through the 
infected fingers of the milkman, in whose 
home a case of typhoid fever exists. Fre- 


TYPHOID FEVER. 


161 


quently it has been found that most cases 
of typhoid developing in a town are on the 
route of one particular milk-wagon. 

( b ) Shell-fish. May carry infection either by hav¬ 

ing lived in contaminated water or by having 
been shipped in water infected with typhoid 
bacilli. 

(c) Vegetables. May carry infection by being 

washed in contaminated water. 

4. Flies. These pests are a great source of the com¬ 
municability of typhoid fever. They alight on the bacil¬ 
lus-laden typhoid stool, and fly away, carrying typhoid 
bacilli on their feet, to deposit them on any article of 
food they may choose for a resting place, or any glass 
of water upon which they may settle. The water or the 
food, upon being taken internally, infects the individual 
with typhoid bacilli. 

5. Clothing. Especially all articles in contact with ty¬ 
phoid patients, such as night-gowns, towels, sheets, pil¬ 
low-cases, blankets, handkerchiefs, etc., which, unless 
carefully disinfected, are fruitful sources for the spread 
of the disease, as they easily become contaminated 
through contact with stools or urine. 

Pathology. The discussion of this subject will be 
limited to a consideration of the intestines and spleen, 
as it is in these two organs that the most characteristic 
changes are found. 

Intestines. These are often distended, and the peri¬ 
toneum over the bowel may show many small hemor¬ 
rhagic areas. Ulcers are to be found in the walls of the 
lower part of the jejunum and ileum, the long axis of the 
ulcers being parallel with the long axis of the bowel. 

A rather detailed consideration of the intestinal ulcera- 
li 


162 


CLINICAL MEDICINE FOR NURSES. 


tion is necessary, in order that the mechanism of two of 
the most important complications of typhoid fever (per¬ 
foration and hemorrhage) may be clearly understood. 

There are four stages in the evolution of the typhoid 
ulcer in the intestinal wall: 

(1) Hyperemia and hyperplasia. 

(2) Necrosis and sloughing. 

(3) Ulceration. 

(4) Cicatrization. 

1. Hyperemia and hyperplasia. This condition is 
characterized by an intense congestion, and by an increase 
in the cells (especially the “lymphoid” cells) in the 
bowel wall, which occurs in the lower part of the 
jejunum and in the ileum, sometimes even extending into 
the large intestine. Peyer’s patches, which are collec¬ 
tions of lymphoid cells normally existing in the bowel 
wall, become greatly enlarged. 

2. Necrosis and Sloughing. A death of tissue in the 
bowel over the affected areas (especially the Peyer’s 
patches or plaques) now occurs. This is due to three 
factors: 

(1) Diminished blood-supply to the involved area 

due to pressure on the blood-vessels running 
in the bowel wall. 

(2) The formation in these vessels of clots known 

as thrombi, which plug the vessels com¬ 
pletely. 

(3) The specific poisoning action of the toxins of 

the typhoid bacillus. 

Necrosis may be superficial or deep. 

3. Ulceration. When necrosis is complete, the slough 
begins to separate from its base, and an ulcer results. 
The separation begins at the edges, and extends inward. 


TYPHOID FEVER. 


163 



until the entire slough is 
cast off. (Perforation 
occurs most frequently 
at the time of the sep¬ 
aration of the slough). 

Several neighboring ul¬ 
cers may unite, forming 
one huge ulcerated area. 

4. Cicatrization. This 
is the stage of repair and 
recovery. It begins as a 
thin film of granulation 
tissue covering the base 
of the ulcer, and grad¬ 
ually extends until all 
signs of damage have 
disappeared. After the 
reparative process is 
complete, the area is 
usually deeper than the 
surrounding tissue, and 
lighter in color. 

The various stages in 
ulcer formation and re¬ 
pair are to be found in 
the bowel at one and the 
same time. Thus, at the 
height of the disease an 
ulcer in the stage of re¬ 
pair may be near one 
that has just reached the stage of necrosis and sloughing. 

Spleen. This organ is always swollen, usually to 
3 times its normal size, due to a tremendous increase in 


Fig. ll —Small intestine. PeyePs plaques showing tumefaction and superficial ulceration. 
Typhoid fever. (From the Pathological Museum of McGill University.) 




164 CLINICAL MEDICINE FOR NURSES. 

the lymphoid tissue, of which it is so largely composed. 

Symptoms. The incubation period in typhoid fever 
is very variable—three to twenty-three days. Roughly 
speaking, about two weeks. 

Onset. This is gradual, the patient feeling below par 
for a week or ten days, suffering from headache, loss of 
appetite, lassitude, increasing weakness and general 
malaise. Nosebleed often occurs. 

Course . The course of typhoid fever is usually 
described by weeks: 

ist Week. The patient feeling badly, finally takes to 
his bed. The temperature rises daily in a step-like man¬ 
ner (see chart), beginning with a maximum of 100°, and 
at the end of the week reaching from 102° to 104°. The 
face is flushed, the eyes bright. There is considerable 
headache, and complete loss of appetite. The tongue is 
coated with a white fur, and frequently dean at the 
edges. The abdomen is moderately distended, and ab¬ 
dominal gurglings are frequent. There is some mental 
dulness. The pulse is full and bounding, and is slow as 
compared with the height of the temperature, running 
usually between 80 and 90 to the minute. Cough with 
some mucoid expectoration is common. The bowels are 
usually constipated, though often there is a simulated 
diarrhea, due to the giving of purgatives. (This must 
not be confounded with “typhoidal diarrhea,” to be men¬ 
tioned later). At the end of the week rose-spots (the 
eruption of typhoid fever) appear either on the abdomen, 
chest or back. They may be few in number or very 
abundant. They are small, pinkish spots, slightly raised 
above the surface of the skin, disappearing at once on 
slight pressure, but reappearing instantly the pressure is 
released. The spleen is usually enlarged. 


* 


TYPHOID FEVER. 



165 


Fig. 12.—Typhoid fever with relapse. (Osier.) 














































































166 


CLINICAL MEDICINE FOR NURSES. 


2 d Week . During this period of the disease the symp¬ 
toms mentioned in the preceding paragraph (with the 
exception of headache, which usually disappears) be¬ 
come more pronounced, and some new ones make their 
appearance. The temperature on the whole is higher, 
running between 102° and 105°, and there are fewer re¬ 
missions. The abdomen may be more distended, and in 
severe cases, diarrhea may set in. The mental condition 
is distinctly more dull than in the first week, the patient 
lying quietly, usually being able to answer questions, but 
paying very little attention to what goes on. Especially 
do patients lose the idea of time, and hence will fre¬ 
quently assert that no food has been given for ten or 
twelve hours, when as a matter of fact such is not the 
case. The pulse becomes more rapid (90 to 110), and 
is often dicrotic. Complications may set in. 

3 d Week. In mild attacks the patient’s condition be¬ 
gins to improve (see 4th week). In severe cases the 
disease is now at its height. The temperature runs 
steadily high (103° to 105°), the abdomen is greatly dis¬ 
tended, the tongue is brown and cracked, sordes appear 
on the lips, the mental condition is profoundly affected, 
some patients being wildly delirious, others lying in a 
stupor. The condition known as “coma vigil” may be 
present, the patient lying with eyes wide open, staring, 
and wholly unconscious. There may be picking at the 
bedclothes. All these symptoms denote intense toxemia, 
and, taken together, are often referred to as the “typhoid 
state.” Emaciation is extreme. The pulse is rapid (120 
or more), weak and thready. There often is diarrhea 
and incontinence of urine and feces. Complications, 
especially perforation and hemorrhage, are particularly 
frequent at this time. 


TYPHOID FEVER. 


167 


4 th Week. If the patient is to survive, improvement 
usually shows itself. Among the first signs are greater 
remissions in the temperature (these occurring usually 
in the morning hours) and betterment in the mental con¬ 
dition, which denotes a lessening of the toxemia. At 
times the temperature may begin to drop, but the mental 
condition fails to clear up; this is a bad sign, denoting 
intense systemic poisoning. The diarrhea lessens, as 
does the abdominal distension; the pulse becomes slower 
and stronger; the dirty, foul tongue clears up, and all 
symptoms abate. By the end of this week convalescence 
is under way. 

In the case of average severity, the patient will be in 
bed about six weeks; mild cases may be up and about in 
a little over a month; while severe cases may be confined 
to bed for three months and more. 

The Urine. The urine' in typhoid fever presents no 
characteristic features other than those usually present 
in any acute febrile disease, save that the diazo-reaction 
of Ehrlich is usually present. During the course of ty¬ 
phoid a very large amount of urine is frequently passed, 
due to the large amount of water forced upon the patient. 

The Blood . The blood in typhoid fever also presents 
no notable changes. The most important fact in connec¬ 
tion with the blood is that the leucocytes are not in¬ 
creased in number , typhoid being one of two common in¬ 
fectious diseases characterized by no increase in those 
cells. The other disease is tuberculosis. In serious cases 
there is, of course, a moderate degree of anemia. 

A word must be said concerning the (< Widal reaction” 
of the blood. This reaction depends upon the presence 
in the blood-serum of substances known as “agglutinins” 
(see chapter on Immunity), which have the power to 


168 


CLINICAL MEDICINE FOR NURSES. 


cause micro-organisms to lose their power of motion (if 
it exists), and of causing them to agglutinate or “clump/’ 
In a patient with typhoid fever specific typhoid agglu¬ 
tinins are present which will cause typhoid bacilli, and no 
others, to clump, and to become motionless. If, for in¬ 
stance, 40 drops of a broth culture of typhoid bacilli are 
mixed with 1 drop of the patient’s blood-serum, and within 
an hour the bacilli are seen under the microscope to lose 
their motility and to clump, the Widal reaction is said to be 
positive in a dilution of 1: 40. If 100 drops of culture are 
mixed with 1 drop of serum, and the reaction is present, it 
is said to be positive in a dilution of 1:100, etc. 

The Widal reaction is an extremely important diagnostic 
point in typhoid fever. It is almost never present until 
the end of the first week, sometimes not until the end of 
the second week, almost always by the third week; hence it 
is of no value at the very beginning of the disease. If the 
patient has been inoculated with antityphoid vaccine within 
three years, the reaction loses its value, as it will almost 
invariably be positive. In view of the very great frequency 
of antityphoid vaccination particularly since the World 
War, the Widal reaction has lost a great part of its diag¬ 
nostic value. 

The Stools. If the stools are not loose, there is nothing 
about them that is characteristic. If they are loose, they 
are generally known as “pea-soup” stools. They are thin, 
of a brownish color, and have a peculiar, characteristic 
odor. On standing, they separate into an upper fluid layer 
and a lower, more solid layer. Constipation is the rule in 
typhoid, and constipated patients seem to do better. The 
early diarrhea is usually due to the giving of purgatives 
before the diagnosis has been made: The late, or typhoidal 
diarrhea is to be classed as a complication. 


TYPHOID FEVER. 


169 


Complications. All the complications of typhoid 
fever cannot be dealt with here, for to do so would require 
almost a separate volume. Those to be mentioned include 
the most frequent and important ones, and those with 
which the nurse will most often be called upon to deal. 

Hemorrhage . Intestinal hemorrhage is caused by the 
erosion or eating away of the wall of one of the blood¬ 
vessels in the bowel by the ulcerative process going on 
in the intestine. Hemorrhage occurs in about 7 per cent, 
of all cases of typhoid fever. The amount of blood lost 
may vary from a few cubic centimeters to a quart, de¬ 
pending upon the size of the injured vessel. When 
hemorrhage is large it is a serious complication. Hemor¬ 
rhages may occur singly or there may be many in rapid 
succession. As a rule, several small hemorrhages prove 
more serious than one moderately large one, for the 
amount of blood lost is greater, and there is less time 
for recuperation. Hemorrhages usually occur at the 
end of the second week and during the third week of the 
disease, but may occur at any time from the onset to con¬ 
valescence. 

The nurse, being with the patient continuously, is the 
one that, far more than the physician, is present at the 
moment the hemorrhage occurs, and should train her 
powers of observation in order to suspect the presence of 
hemorrhage at the earliest possible moment. 

Symptoms. A small hemorrhage, a couple of ounces 
or so, as a rule, gives no symptoms, and is not even sus¬ 
pected until the blood is passed in the stool. With a 
larger hemorrhage there may or may not be abdominal 
pain at the time of bleeding. If the hemorrhage is 
copious there is usually a sudden fall in temperature , a 


170 


CLINICAL MEDICINE FOR NURSES. 


sense of weakness, and, in marked cases, pallor, with a 
cold sweat, restlessness and “air-hunger/’ the patient 
complaining of a stifling sensation, and restlessly tossing 
the head from side to side on the pillow. There is usu¬ 
ally a change in the pulse at the time of bleeding; it be¬ 
comes faster, and has a peculiar “bounding” feel, diffi¬ 
cult to describe but easy to recognize when once its sig¬ 
nificance has been appreciated. The main thing for the 
nurse to note is the change, not alone in the pulse, but in 
the patient’s general condition. 

The above symptoms permit only the suspicion of 
hemorrhage. Proof comes when the blood is passed 
from the bowel. Usually the blood is dark and clotted, 
though if the hemorrhage is profuse and low down in the 
bowel the blood passed may be a brighter red. It is only 
by constant watchfulness that the nurse will be able to 
detect the early signs that are suggestive of hemorrhage; 
but by their prompt detection and interpretation, and by 
carrying out at once the provisional orders left by the 
physician, she will do much towards aiding her patient 
in his fight for life. 

Perforation. Perforation is the most serious and most 
dreaded of all the complications of typhoid fever. It is 
brought about by the eating away, through deep ulcera¬ 
tion, of the peritoneum covering the bowel. Immediately 
after the perforation has occurred, the infectious bowel 
contents are flowing freely into the peritoneal cavity, 
setting up an acute general spreading septic peritonitis. 
In the absence of prompt diagnosis and speedy surgical 
interference, death is inevitable. 

No nurse is ever required or desired to make a diag¬ 
nosis of perforation, but she must be on the alert for 
those symptoms suggestive of the condition, in order that 


TYPHOID FEVER. 


171 


she may at once summon the physician. If she is in 
doubt, she should always call the doctor. It is better to 
send for him a dozen times on false alarms than to hesi¬ 
tate and delay when the real danger is present, for in 
cases of perforation minutes count. 

Perforation occurs in 2 per cent, to 3 per cent, of all 
cases, and usually during the third week, though, as in 
the case of hemorrhage, it must never be forgotten that 
it may occur at any time. 

Symptoms. By far the most important single symp¬ 
tom of perforation is sudden severe paroxysmal abdom¬ 
inal pain. Nausea and vomiting, sweating and signs of 
collapse may occur. Any sudden and obscure change in 
the patient’s condition is suggestive. After perforation 
the pulse tension rises (the opposite from hemorrhage), 
and eventually the “wiry” pulse of peritonitis is to be 
felt. From the standpoint of the nurse, pain is by far 
the most important symptom. The leukocytes are in¬ 
creased in number with the development of peritonitis, 
which is an important aid to the physician in making the 
diagnosis, as in uncomplicated typhoid there is no leu¬ 
kocytosis. If surgical intervention is not resorted to, 
the symptoms of general peritonitis will manifest them¬ 
selves. 

Thrombosis. This complication frequently occurs, usu¬ 
ally in the femoral or iliac vein. When in the femoral 
vein, there is pain down the leg, usually some swelling, 
edema and cyanosis, and the vein may be felt as a hard, 
tender cord. When thrombosis occurs in the iliac vein, 
the pain is abdominal, and owing to its severity m^y 
suggest perforation. 

Lobar Pneumonia. This disease may occur as a com¬ 
plication of typhoid fever. Attention is called to the 


172 


CLINICAL MEDICINE FOR NURSES. 


chest by pain, cough, and rusty sputum. The tempera¬ 
ture may rise, though if it is very high at the time of the 
onset of pneumonia no change may be observed. The 
leukocytes are increased in number. 

Myocarditis. This condition occurs in a measure in 
practically every severe case of typhoid fever where the 
patient is profoundly poisoned and the heart suffers from 
the effects of toxemia. The symptoms are not char¬ 
acteristic, weakness and some irregularity of the pulse 
being the main signs to be detected by the nurse. 

Tender Toes. Frequently at the height of the disease, 
or during its latter portion, the tips and under surface 
of the toes become exquisitely tender, so much so that 
the weight of the bedclothes produces intolerable suffer¬ 
ing. The condition is probably due to an irritation of 
the sensory nerve-endings. 

Abscesses. These occur frequently, and no part of 
the body is immune from invasion. Typhoid bacilli are 
sometimes found in the pus. The symptoms vary so 
widely with the location of the abscess that no detailed 
description can here be given. In almost every case 
there is local pain, heat, redness and swelling (if the ab¬ 
scess is on the surface of the body), a rise in tempera¬ 
ture, and at times the appearance of chills and sweats. 

Diarrhea. This occurs at the end of the second or 
during the third week, and is a serious complication, be¬ 
ing due to profound toxemia and deep intestinal ulcera¬ 
tion. The stools may number from four to ten per day, 
and because of their frequency prove a great additional 
drain upon a patient already overwhelmed with poison. 

Relapse. By relapse in typhoid fever is meant a recur¬ 
rence of the symptoms of the disease after the tempera¬ 
ture has been normal for five or six days. The relapse 


TYPHOID FEVER. 


173 


resembles in every way the original attack, save that it is 
usually much shorter and milder, though in no sense free 
from danger, as it attacks a patient already exhausted. 
A new crop of rose-spots may appear, the spleen again 
becomes enlarged, and any of the complications of ty¬ 
phoid, whether present before or not, may occur. 

Prognosis. The forecast in typhoid fever must al¬ 
ways be guarded, the saying of Hippocrates being very 
appropriate: “In acute disease it is not safe to prophesy 
either death or recovery/’ 

Death-rate is highest under 2 years of age. 

Death-rate is lowest from 2 to 15 years of age. 

Death-rate is lower from 15 to 25 than from 25 to 40. 

Death-rate is higher over 40. 

Generally speaking, the mortality is from 7 per cent, 
to 10 per cent. 

The following elements are to be considered in esti¬ 
mating the patient’s chances for recovery: 

1. Toxemia. If it appears early, it is serious. If the 
patient refuses nourishment, and especially water, the 
outlook is grave. 

2. Nervous symptoms—delirium, etc.—if occurring 
early, are of bad omen. 

3. Pulse. Any rate over 120, save if very temporary, 
is a bad sign. Irregularity is always serious. 

4. Lung complications. Pneumonia is very fatal. 

5. Abdominal distension (meteorism), if marked, is 
a bad sign, as it indicates intense toxemia. 

6. Diarrhea. Always a bad sign, indicating severe 
toxemia. 

7. Hemorrhage. Needs no further discussion. 

8. Perforation. “Recovery without operation is hardly 
to be credited.” 


174 


CLINICAL MEDICINE FOR NURSES. 


Prophylaxis. General municipal measures for the 
control of the typhoid situation and for the prevention 
of its spread, when once present, do not concern us here. 

Special Measures in Connection with 
the Patient. 

Typhoid fever is a preventable disease, for every ty¬ 
phoid bacillus is within our power and under our control 
at the time it leaves the human body. Typhoid fever 
does not originate spontaneously, and every case must 
come from a pre-existing source. Consequently, if every 
typhoid bacillus were destroyed at the time it is cast off 
from the human body, the disease would soon be almost 
eradicated. 

The preventive measures, presently to be enumerated 
and described, concern the nurse more than anyone else 
for two reasons: first, for her own protection; second, 
because she is the one that must carry them out, and it is 
due to her conscientiousness and never-slacking attention 
that the measures prove efficient. The physician in 
charge of a case leaves his orders as to prophylactic 
measures; but if the nurse does not whole-heartedly and 
scrupulously execute them, they are practically of no 
value. 

(a) Isolation. While of course this is not as neces¬ 
sary as in smallpox or diphtheria, yet the patient with ty¬ 
phoid fever should be alone, save for the nurse, as much 
as possible. There is no greater mistake than to allow 
members of the family to come in, sit down and talk with 
the patient simply because the case is not a desperate one. 
The room should be arranged with due regard to attract¬ 
iveness, but all heavy window draperies, carpets, etc., 


TYPHOID FEVER. I 75 

should be removed. There should be nothing in the room 
that cannot be easily and thoroughly cleaned. 

( b ) Disinfection of the following: 

(1) Stools. 

(2) Urine. 

(3) Sputum and vomitus. 

(4) Clothing and bedding. 

(5) Bedpans, urinals, thermometers, syringe- 

nozzles, etc. 

1. Stools. Each physician has his own choice of the 
particular disinfectant to be used. The following are • 
the agents most in use at present: 

(1) Bleaching powder . 3 per cent, solution 

(2) Milk of lime . 1.8 “ “ 

(3) Cresol . 1 

(4) Carbolic acid. 5 “ 

(5) Formalin . 10 “ 

No matter which is used, the stool should be received 
into a bedpan containing some of the gennicide, and 
after the patient has finished with the bedpan, enough of 
the disinfectant should be added to secure twice as much 
disinfectant as there is stool. Solid clumps of feces 
should be broken up with a rod, and the whole mass 
thoroughly stirred and set aside, protected from flies, 
for two hours before being disposed of. 

2. Urine. Bichloride of mercury is the* best disin¬ 
fectant. A 1: 1000 solution is used, there being at least 
% 0 as much of the bichloride solution as there is urine; 
thus, 1 ounce of bichloride solution will disinfect 40 
ounces of urine. It is best to keep the bichloride solution 
in a large jar, and pour the urine into that from the bed 
urinal, the jar being emptied daily. The mixture of bi¬ 
chloride and urine should stand for at least two hours 
before being thrown away. 







176 


CLINICAL MEDICINE FOR NURSES. 


3. Sputum and vomitus. Neither of these is ordi¬ 
narily obtained in typhoid fever, but when present the 
sputum should be received in a sputum cup and burned, 
while the vomitus can be disinfected with the same 
germicide used for the stools. 

4. Clothing and bedding. Gowns, sheets, pillow-cases, 
etc., can be soaked in 5 per cent, carbolic acid or 10 per 
cent, formalin for two hours; then boiled. Rubber sheets 
to be soaked in carbolic, as boiling is injurious to them. 

5. Bed-pans, urinals, etc. Fill pans or jars with agent 
used for stools, then scald in water. Boil all enema 
tubes, syringes, nozzles, etc.; keep the thermometer in a 
glass or small bottle containing carbolic 5 per cent, or 
formalin 10 per cent. 

See to it that the patient has separate dishes, glasses, 
silverware, napkins. If possible, select some dishes and 
silver of a different pattern from that used by the rest 
of the household, in order to prevent mistakes occurring. 

Precautions on the Part of Attendants. 

Great care is an absolute necessity. A basin of bi¬ 
chloride (1: 1000) should be at hand, as well as plenty 
of hot water and soap. Whenever the nurse has been 
busy with the patient—bathing, giving an enema, making 
the bed, cleansing the buttocks after a sto6l, etc.—she 
should carefully wash her hands with water, soap and a 
brush, and then immerse the hands for three minutes in 
bichloride. Remember that every germicide takes time 
to act, and do not be misled as to the efficacy of the pale- 
blue solution to the extent of believing that dabbing the 
tips of the fingers therein ensures absolute sterilization. 
Be sure to have a basin of bichloride and a clean towel 
for the doctor whenever he calls. 


TYPHOID FEVER. 


177 


When nursing a case of typhoid fever in a private 
house, try in every way to avoid having anything what¬ 
soever to do with the preparation or handling of the food 
for the rest of the family; try, if possible, not to have 
to go to the ice-chest; have a little refrigerator for the 
exclusive use of the patient. If such arrangements can¬ 
not be made, cleanse the hands with scrupulous care be¬ 
fore touching any food whatsoever. 

These precautions entail much hard work, but their 
never-failing observance places the trained nurse where 
she rightly belongs—in the position of a power for good 
in the community and in the family; and, in addition, 
her preventive labors will greatly lessen her own chances 
of developing typhoid fever. 

Preventive Typhoid Inoculation. An active immunity 
to typhoid fever can be brought about by the injection of 
dead typhoid bacilli. “The procedure is harmless, 
rational, and effective” (Rosenau). 

Preventive inoculation against typhoid is a procedure 
to which every nurse should submit. 

The vaccine is made from a twenty-four-hour broth 
culture of typhoid bacilli killed by being heated to 60° C. 
for one hour. Injections are given every ten days for 
three doses, between 50,000,000 and 500,000,000 dead 
bacilli being injected at each dose. There may be mod¬ 
erate evidences of reaction: soreness with pain, heat, 
redness and swelling at the site of injection, a moderate 
rise in temperature, or a feeling of general malaise. 
These symptoms appear within twenty-four hours after 
the injection, and usually subside within 24 to 36 hours 
after their onset. The immunity conferred lasts from 
three to four years, and may be indefinitely continued by 
further inoculations. 


178 CLINICAL MEDICINE FOR NURSES. 

“As a striking instance of the protection offered by 
vaccination against typhoid may be quoted the result in 
the United States Army during the maneuvers around 
San Antonio, Texas, in the summer of 1911. 

“All the men, numbering 12,801, were inoculated. 
From March 10th to May 10th, two cases of typhoid 
fever occurred, both patients recovering. One patient 
was a private in the hospital .corps who had not com¬ 
pleted the series of inoculations, having had but two 
doses; the other was a teamster who had not been inocu¬ 
lated. Among the 12,801 men there were but 11 deaths 
from all diseases. Typhoid fever was prevalent at this 
time in the neighborhood. In the city of San Antonio 
there were 49 cases, with 19 deaths” (Rosenau). The 
most convincing proof of the effectiveness of antityphoid 
vaccination is to be found in the vaccination of some 
5,000,000 men in the U. S. Army during the World War, 
as a result of which less than 200 developed typhoid. 

Treatment. Typhoid fever is a self-limited disease, 
and we have no means at our command with which to 
shorten the attack. As*in the case of the great majority 
of maladies, we are unable to treat the disease itself. 
We must devote our time and care to treating the pa¬ 
tient that is suffering from the disease. 

While every physician prefers a certain routine treat¬ 
ment in typhoid fever, especially as regards the diet, there 
are certain fundamental principles so generally accepted 
and practised that many or all of them will be made use 
of in by far the greater number of cases. 

Rest. Absolute rest in bed in the recumbent position, 
with use of bed-pan and bed-urinal, are essentials through¬ 
out the course of the disease, and well into convalescence. 

Diet. There are almost as many diets for typhoid as 


TYPHOID FEVER. 


179 


there are physicians treating the disease. The “diets” 
vary from that of certain German authorities who with¬ 
hold practically everything save water, to the advocates 
of the “high-calorie” diet, which is decidedly liberal. The 
diet in typhoid fever will be dealt with generally, no hard- 
and-fast rules being laid down (for none really exist), the 
author contenting himself with registering his decided per¬ 
sonal preference for the more liberal methods of feeding. 

Liquid Diet. This is probably the most used. Reliance 
is placed on the following articles: 

Milk. Four to 6 ounces every four hours, to which 
are added 2 ounces of lime-water. 

Egg-albumen. The whites of 2 eggs every four 
hours, alternating with the milk. 

Thus the patient receives nourishment every two hours. 

Many patients will successfully weather an attack of 
typhoid on these two articles of food. If the milk dis¬ 
agrees, or if the patient tires of it, buttermilk, whey, 
koumiss, or even peptonized milk can be tried. Milk may 
also be taken with ease by many if the taste is disguised 
by the addition of a very small amount of tea or coffee. 

Ice-cream is a very satisfactory food, being nutritious, 
palatable, and readily taken, especially by children. 

Clear soups are permissible, but must be taken in addi¬ 
tion to, and not instead of, other food. Their taste is 
pleasant, but their nutritive value, is slight. 

Tea and coffee are usually allowed in moderation, 
unless in the opinion of the physician there exists some 
contraindication. Beef broths and artificially prepared 
foods are, as a rule, not necessary; if the patient can take 
food at all, he can take natural foods. 

While it is an every-day clinical fact that hundreds of 
patients do well on the scheme of diet sketched above, the 


180 


CLINICAL MEDICINE FOR NURSES. 


advocates of more liberal feeding claim that by this method 
the patient is less emaciated, less exhausted, and more 
rapidly convalescent. 

Referring to the chapter on “Foods and Nutrition” it 
will be seen that an average individual weighing 70 Kg. 
(154 lbs.) needs practically 2200 calories of food in 
twenty-four hours while in a state of health. When a 
victim of fever, from whatever cause, the tissues of the 
body are consumed (oxidized) more rapidly than nor¬ 
mally, and consequently an overplus of food is necessary. 

Under a strictly milk diet, assuming that the patient 
takes 2 quarts daily, the twenty-four-hour total is but 
1300 calories. The advocates of the high-calorie diet 
which has been championed and elaborated mainly by 
Drs. Warren Coleman, of New York, and Shattuck, of 
Boston, believe in pushing the caloric value of the diet 
up to 3000 calories in twenty-four hours, and, if this is 
well borne, even exceeding that amount, sometimes reach¬ 
ing 4000 to 5000 calories during convalescence. 

The following table shows the variety of foods allowed, 
together with their caloric value: 


Name 

Amount • 

Calories 

Apple sauce. 



Bread . 

..average slice. 

. 80 

Butter . 



Cereal . 



Crackers. 


. 114 

Cream, 20 per cent. . 



Eggs, whole. 



Egg, white. 



Egg, yolk. 



Lactose . 

... .oz. . 

36 

Milk, whole. 

.pint. 


Potato, whole. 


. 90 

Potato, mashed ... 



Rice, boiled .. 

.oz. X A . 

60 

Sugar-cane. 


. 16 

Toast . 

..average slice. 

. 80 





























TYPHOID FEVER. 


181 


With this table at their command, physician and nurse 
can work together and keep a very accurate record of the 
actual fuel value of the food the patient is getting. No 
set rules can be given for the administration of the diet. 
The patient is to take all he can, but is not to be forced 
beyond the limits of comfort. 

Ardent advocates of this form of diet claim: 

No marked emaciation. 

No typhoid state. 

Many patients able to read and divert themselves 
during their illness. 

Patients able to be up and about sooner, and feel 
stronger. 

A quotation from an article by Dr. Coleman is here 
appropriate: 

“The physician should possess at least a rudimentary 
knowledge of the caloric value of food. But probably 
the chief requisite to the successful administration of the 
diet is intelligent co-operation on the part of the nurse * 
Where a nurse is trained in the use of the diet, general 
directions regarding the total number of calories will 
suffice. At her discretion, she will increase or lessen the 
total amount of food or of particular articles while await¬ 
ing further instructions. When a nurse is not trained 
in the use of the diet, the physician himself must assume 
immediate control of the feeding/’ 

Water. Equal to, if not surpassing the diet in impor¬ 
tance, is the amount of water taken by the patient. Too 
much water can hardly be given, for by its diuretic action 
it flushes out the kidneys, and, in addition, by its pres¬ 
ence in the tissues it serves to dilute and thus render less 


* Italics are mine. 



182 CLINICAL MEDICINE FOR NURSES. 


harmful the toxins of the typhoid bacillus. Practically 
all authorities agree that at least 2 quarts of water should 
be taken in twenty-four hours, and many prefer their 
patients to take, as nearly as possible, 100 ounces (a little 
over 3 quarts) daily. The nurse must exercise vigilance 
and patience in order to persuade the patient to take the 
requisite amount of water, but such efforts are well re¬ 
paid, for water is unquestionably the best “medicine” for 
typhoid fever. 

Hydrotherapy. While the previous paragraph may 
well be termed “internal hydrotherapy,” “external hy¬ 
drotherapy” is probably the one most important method 
of treating typhoid fever. 

Hydrotherapy is practised in three ways: 

(1) Sponges. 

(2) Packs. 

(3) Tub baths. 

In hospital practice tub baths are generally preferred. 
In private practice, because of the number of attendants 
required to give the tub bath, and because of the diffi¬ 
culty in securing a portable tub, sponges and packs are 
usually resorted to. The effect of all three is the same, 
the tub bath being probably the most efficient. 

Each physician has his own rule for the indications for 
hydrotherapy. In some hospitals the routine order is a 
tub bath every three hours when the temperature is over 
102.5°. Baths, packs or sponges are given for from ten 
to twenty minutes, the first ones given being usually 
shorter. When the sponge or pack is used, the tempera¬ 
ture of the water is usually about 70° F., though that may 
be altered in each individual case. For the first tub bath, 
the temperature of the water is generally not under 85° 
F., and the bath is never given at a lower temperature 
than 65° F. 


TYPHOID FEVER. 


183 


It is not the intention of the author to go into the de¬ 
tails of the technique of giving sponges, packs or tub 
baths, as that more properly comes under the head of 
“practical nursing,” and the teaching of each training 
school varies in some of the details of the procedure. 

Advantages of hydrotherapy: 

( a ) Toxemia lessened—probably the most important 
feature. Patients practically comatose when the bath is 
begun can, at the end of ten or fifteen minutes, answer 
questions fairly intelligently. The “typhoid state” is 
more rarely seen under the use of the baths. Delirium 
and tremor are lessened, and there is lessened absorption 
and increased elimination of toxins. 

( b ) Temperature reduced. Contrary to the general 
supposition among the laity, reduction in temperature, 
while desirable and welcome, is essentially not one of the 
chief objects of the baths. At the height of the disease 
the temperature may be but very slightly influenced (less 
than one degree), yet the general condition may be very 
markedly benefited. 

(c) Circulation. The vasomotor system is stimulated 
—the general tone of the vessels is raised. The heart- 
rate is lessened, the pulse is made smaller and harder, and 
blood-pressure is raised. 

(d) Respiration. With each bath or pack the patient 
takes a few full, deep breaths, and thoroughly expands the 
lungs. This lessens the danger of passive congestion at 
their bases in the deep hollows present on either side of 
the spine and thus diminishes the likelihood of hypostatic 
pneumonia. 

(e) Digestion. Disturbances of this function are less 
common, and the mouth is usually in better condition, 
due to lessened toxemia. 


184 


CLINICAL MEDICINE FOR NURSES. 


(/) Skin. Liability to bed-sores is decreased. 

( g ) Mortality is lowered 5 to 7 per cent. 

Contra-indications to hydrotherapy: Baths should not 
be given in the presence of: 

(1) Abdominal pain. 

(2) Hemorrhage. 

(3) Perforation. 

(4) Phlebitis. 

(5) Great prostration with failing circulation. 

(6) Any serious complication. 

General Measures. The care of the mouth is all-im¬ 
portant, and scrupulous attention on the part of the 
nurse to this disagreeable duty will often result in avoid¬ 
ance of the dry, brown, cracked, fissured tongue, the 
sordes on the lips, and in lessening the bad taste and 
general “cottony” feeling of the patient’s mouth. 

The mouth should be cleansed after each feeding, and 
special attention should be devoted to the tongue. Some 
good mouth-wash is desirable, and tooth-picks with the 
end wrapped in cotton can be dipped in this and rubbed 
over the teeth and gums. The lips should be frequently 
moistened with glycerine, vaseline, or some softening and 
soothing ointment. The care the nurse takes of her 
patient’s mouth is a pretty good index of the general 
attention that patient is getting. 

The care of the skin is also very important. Fre¬ 
quent alcohol rubs should be given, after which a dust¬ 
ing powder should be applied. After each stool the but¬ 
tocks should be sponged with carbolic acid (1:40) solu¬ 
tion, and then freely powdered, care being taken to get 
the powder well into the natal cleft. At the slightest ap¬ 
pearance of redness or irritation on the skin, pressure 
should at once be relieved by means of a rubber or cot- 


TYPHOID FEVER. 


185 


ton ring, and the physician’s attention directed to the 
irritated area, that he may deal with it as he sees fit. 

Frequent change of position is very essential, as it les¬ 
sens the chances of passive congestion in the lungs, and 
also lessens the occurrence of bed-sores. Patients that 
are not very ill will change position of their own free 
will, but the stuporous patient will lie for days flat on 
his back. Such individuals must be rolled on the side 
(first on one side, then on the other) two or three times 
daily for half an hour at a stretch, and retained in 
that position by means of pillows, bolsters or sand-bags. 
See that the patient voids plenty of urine, and that the 
bladder does not become overdistended, which can easily 
happen in stuporous patients. 

Routine Drug Treatment. Generally speaking, there is 
none in typhoid, drugs being used only to meet special 
conditions as they arise. The one exception to this rule 
is the use of hexamethylenamin (urotropin) in 5-grain 
doses three times daily to render the urine sterile. 

Treatment of complications. 

1. Hemorrhage. The usual routine is: 

Discontinue all food until told to resume it by the 

physician in charge. 

Discontinue stimulants if they are being given. 

Give morphia grain with atropin % 50 grain hy¬ 
podermically. 

Do not move bowels for three days; then give an oil 
enema, to be followed by a soapsuds enema. 

Other measures as indicated by the physician. 

2. Perforation. Immediate operation is the only 

treatment. 

3. Thrombosis. Place the leg at absolute rest on a pil¬ 
low. Move only when necessary, and then with the 
greatest care. 


186 


CLINICAL MEDICINE FOR NURSES. 


Do not rub the leg, as by doing so bits of the clot in 
the vein may be detached, float about in the circulation, 
and by their final lodgment cause the death of the patient. 

4. Failing Heart. The methods of combating heart 
weakness are so varied that it is impossible to go into 
them in detail. In the event of sudden collapse, treatment 
is similar to that given in detail in the chapter on Lobar 
Pneumonia ( q.v .). 

5. Meteorism. A simple diet and plenty of water les¬ 
sen the occurrence of this distressing condition. When 
it is present, food is discontinued (save water), and 
turpentine is administered in the form of stupes, and by 
enema. 

6. Diarrhea. Diet cut to albumin water. Drugs as 
seen fit by the physician; bismuth and lead acetate those 
most in use. Starch and laudanum enema sometimes 
given. 

Managment of other conditions. 

(а) Toxemia. Water, inside and out, is the best 
treatment. In addition to the water taken by mouth, salt 
solution may be introduced by rectum (Murphy drip), 
under the skin (hypodermoclysis), or into a vein (in¬ 
fusion). It may be necessary to feed the patient by 
means of a stomach-tube. 

(б) Headache. This condition is prominent usually 
only during the first week, and is generally best controlled 
by the use of the ice-bag. It may become necessary to 
use drugs, such as codeine. 

(c) Delirium. Being one of the manifestations of 
toxemia, the free use of water is the best mode of treat¬ 
ment. When delirium is continued, active, and is ex¬ 
hausting the patient, a good dose of morphia hypoder¬ 
mically produces the best results. At times delirium is 


TYPHOID FEVER. 


187 


so violent as to necessitate hyoscin, while at others, bro¬ 
mides will control it satisfactorily. 

( d ) Constipation. Distinctly desirable. Aside from 
moving the bowels daily by enema, nothing should be 
done to interfere with it. 

( e ) Abdominal Pain. Must always be looked upon 
as possibly a symptom of a serious complication. Heat 
or cold will often relieve. It is not looked upon as wise 
to give morphia for the relief of abdominal pain in 
typhoid fever. 

(/) Tender Toes. Remove pressure by making cradle 
(use-barrel hoops if necessary) over the feet so that they 
will not come in contact with the bedclothes. 

Convalescence. When the temperature has been 
normal for about a week, the patient is usually allowed 
to be propped up in bed, and three or four days later can 
be placed in a chair, beginning to walk when strength 
permits. The appetite of convalescing typhoid patients 
is proverbially large, and care must be exercised lest they 
over-eat in their enthusiasm. The individual steps in con¬ 
valescence vary so with the particular case that their 
enumeration or description is impossible. 

General points in treatment. 

1. Absolute rest—as much isolation as possible. 

2. Simple, but not necessarily meager, diet. 

3. Water in abundance: 

(a) Inside. 

( b ) Outside—packs, sponges, baths. 

4. Bowels to be let alone if not too loose. 

5. Drugs only for special conditions—none as a routine, 
save hexamethylenamin (urotropin) to destroy typhoid 
bacilli in urine. 

6. Constant, never-ceasing vigilance. 


CHAPTER XXII. 

TUBERCULOSIS. 

There are many books on tuberculosis for laymen, 
nurses and physicians where more detailed accounts of this 
scourge can be found than the limits of these lectures will 
permit. Here the subject must be at least sketchily traced. 

Tuberculosis is an infectious disease caused by the 
tubercle bacillus. It is the most widespread and the most 
frequent serious disease of the human race, one death in 
seven, from all causes, being due to it. Tuberculosis may 
attack any and every portion of the body, certain or¬ 
gans and structures such as the lungs, lymphatic glands, 
and joints being particularly susceptible. No matter what 
organ or structure is attacked, the fundamental cause is 
one and the same (the bacillus of tuberculosis), and the 
pathological process is also the same. Tuberculosis of the 
glands, joints, bones, etc., are known as cases of “surgical 
tuberculosis.” These conditions will not be considered. 
In this chapter will be taken up what might be termed 
“medical tuberculosis,” i.e., tuberculosis of the lungs and 
the most frequent tuberculous complications of a medical 
nature that are met with. 

Historical Note. Pulmonary tuberculosis has been 
known to man from the most remote times. Babylonian 
records, the most ancient known, make mention of it. 
Hippocrates (b. c. 460-376) gives an intelligent descrip¬ 
tion of the disease. Aristotle, a contemporary of Hippo¬ 
crates, notes that it was a general belief among the 
Greeks that phthisis or consumption was contagious. No 
advance was made with regard to the nature of the dis¬ 
ease for 1400 years, when anatomical study began. 
Sylvius (1695) first indicated the connection between 
■ (188) 


TUBERCULOSIS. 


189 


tuberculosis nodules and phthisis. Morton (1689) 
brought the tubercle prominently to attention as the 
true cause of phthisis. Stark (1785) accurately de¬ 
scribed miliary tubercles, and paved the way for the 
correct understanding of their nature and relation to 
phthisis. Bayle (1803) studied miliary tubercles in all 
stages, stressed the importance of differentiating young 
from old tubercles by differences in their opacity, and 
claimed that true tuberculosis is a constitutional affection 
which can cause development of nodules in all organs, 
and not originate in inflammation, although often com¬ 
plicated with it. 

“Laennec (1819), whose work soon followed Bayle’s, 
consummated and simplified the knowledge thus far 
gained. He recognized the unity of all phthisis as tuber¬ 
culosis, and scrofula as tuberculosis of lymph-glands; 
his ideas in general as to causation and infection were 
distinctly modern, and his description of the tubercle and 
its transformation toward ulceration are unexcelled. 
Most valuable of all was his gift of the art of ausculta¬ 
tion. No genius like that of Laennec so far anticipated 
his own day” (Baldwin). 

In December, 1865, Villemin presented his paper “On 
the Cause and Nature of Tuberculosis and the Inocula¬ 
tion of the Same from Man to Rabbit.” His conclusions 
were as follows: 

“1. Tuberculosis is a specific affection. 

“2. It has its origin in an inoculable agent. 

“3. The inoculation from man to rabbits is very suc¬ 
cessful. 

“4. Tuberculosis pertains, therefore, to the virulent 
diseases, and should be classed with variola, scarlatina, 
syphilis, or, better still, with glanders.” 


190 


CLINICAL MEDICINE FOR NURSES. 


Villemin employed many different elements for his 
inoculation experiments, among them being fragments 
of lung tubercle, sputum, blood, tuberculous glands, 
tubercle from cattle (bovine tubercle), and obtained 
positive results (i.e., development of tuberculosis in the 
rabbit) in almost all cases. 

Finally, in 1882 Robert Koch, Health Officer in an 
obscure German town, discovered the tubercle bacillus, 
and proved conclusively that it was the sole cause of 
any and every form of tuberculosis. • 

Etiology. The sole cause of tuberculosis is the 
tubercle bacillus. It belongs to the vegetable kingdom, 
and when seen in stained preparations appears as a small, 
straight, or slightly curved red rod. 

The tubercle bacillus requires the presence of oxygen 
in order to develop. It grows best at body temperature 
(98.6° F., or 37° C.). Temperatures below 30° C. or 
above 42° C. markedly lessen its growth. Direct sun¬ 
light kills the germ in a few hours. Five per cent, car¬ 
bolic acid kills it in a few minutes; but when the bacillus 
is embedded in sputum, five or six hours are often neces¬ 
sary to kill all the organisms. 

Modes of Infection. It is now the opinion of most 
authorities that infection with the tubercle bacillus takes 
place in childhood, usually before the tenth year. The 
bacilli may gain entrance into the body by two routes: 

1. Inhalation—being breathed in with the air. 

2. Ingestion—being taken into the intestinal tract with 
food. 

No matter how the bacillus finds an entrance, it quickly 
goes to lodge in the mesenteric lymph-glands that lie at 
the back of the abdomen near the spine, or in the 
mediastinal or bronchial lymph-glands situated in the 


TUBERCULOSIS. 


191 


chest around and between the roots of the lungs. In 
these glands the tubercle bacilli may lie for years, and in 
fact for a lifetime, without causing any symptoms. If, 
however, for any reason the resisting powers of the body 
are markedly lowered, the bacilli take advantage of this, 
and by the action of their poisons, as well as of their 
bodies, gain the upper hand. They most frequently mi¬ 
grate to the lungs, which are the organs in the body 
most susceptible to their inroads. Symptoms then make 
their appearance, and the individual becomes ill with 
tuberculosis. 

It is important to stress the difference between “tuber¬ 
culous infection” and “tuberculous disease.” Every in¬ 
dividual harboring tubercle bacilli in his body is the vic¬ 
tim of “tuberculous infection.” It has been proven from 
countless autopsies in large general hospitals that, of in¬ 
dividuals dying from all causes, over 85 per cent, showed 
signs of “tuberculous infection.” On the other hand, an 
individual is not the victim of “tuberculous disease” 
until symptoms appear that warrant a diagnosis of 
tuberculosis. 

Contributory causative factors. 

1. Heredity. In the past the influence of heredity was 
greatly overestimated. We now know that a child born 
tuberculous (the only way in which the disease can be 
really inherited) is so rare as to be a curiosity. Heredity, 
however, is not to be set aside, for it does pass on to the 
child a predisposition to infection with the tubercle bac¬ 
illus, and also a lack of resisting power to the bacillus 
when once infected. Consequently, individuals in whose 
family history there is a marked tuberculous strain are 
far more likely to succumb to the disease than are those 
whose family tree is unscathed. 


192 


CLINICAL MEDICINE FOR NURSES. 


2. Environment. Far more important in determining 
the outbreak of pulmonary tuberculosis are the environ¬ 
ment and habits of the individual. These can best be 
considered under several sub-headings: 

(a) Dissipation. “Wine, woman, and song” furnish 

a good soil for the development of tuber¬ 
culosis. 

( b ) Lack of air in the home, the office or the work¬ 

shop. Tuberculosis is essentially a “house 
disease,” and prolonged residence in badly 
ventilated quarters greatly lowers resistance. 

(c) Overwork. ") 

( d) Insufficient food, v All lower bodily resistance. 

(e) Smoke and dust. I 

(/) Prolonged contact with tuberculous individ¬ 
uals that expectorate carelessly and promis¬ 
cuously. 

( g ) Lack of light and sunshine. Tubercle bacilli 
that have been expectorated grow and multiply best 
under these conditions. 

Pathology. 

The Tubercle. No matter where the tubercle bacillus 
shows its activities, the result is the same—the tubercle. 

To the naked eye the tubercle is a small pearly-gray 
mass about the size of a pin-head. Tubercles in the 
affected area may be scattered, and at a distance from 
each other, or so close to one another as to leave no 
appreciable space between. Several tubercles may join to¬ 
gether or coalesce. While the young tubercle is pearly- 
gray, the older tubercles lose this color, and become 
opaque and whitish in the centre. This occurs because 
the toxins of the tubercle bacillus act so as to block off 
the minute blood-vessels going to the portion of the 


TUBERCULOSIS. 


193 


organ that is invaded, and thus the blood supply is cut 
off. In the absence of blood supply there must, of 
course, be death of tissue. The tuberculous tissue under¬ 
goes a process known as “caseous degeneration” or 
“caseation”— i.e. } a degeneration into a cheesy mass, hav¬ 
ing no definite structure. When this occurs in the lungs 
to any great extent, the cheesy, decayed matter is thrown 
off in the sputum, and a cavity is the result, the cavity 
being nature’s attempt at safeguarding the body by get¬ 
ting rid of decayed tissue that is no longer of any use, 
and leaving in its place a cavity or “hole” which nature 
again attempts to safeguard by weaving about it a cap¬ 
sule of dense, fibrous tissue, in order to wall it off. 

Types of tuberculosis. 

Acute General Miliary Tuberculosis. This condition, 
as the name implies, consists in an invasion of the entire 
body by the tubercle bacillus. It usually occurs when, 
from some known or unsuspected focus of tuberculosis, 
a large number of bacilli are set free at once in the 
blood-stream. The body has no time to marshall its 
defensive resources, and is overcome by the extent and 
intensity of the infection. Miliary tubercles are to be 
found scattered throughout the body—in the lungs, 
brain, liver, spleen and other organs. 

Symptoms. These are vague, as far as the possibil¬ 
ity of diagnosis is concerned, for there are practically 
none that point to tuberculosis. The picture is one of 
intense general sepsis, and at first is frequently mistaken 
for typhoid fever. The temperature is irregular, show¬ 
ing marked variations (in one case seen by the writer 
the minimum in twenty-four hours was 96° and the 
maximum 106°) ; there are frequent chills and abundant 
sweats, accompanied by rapid and profound emaciation. 


13 


194 


CLINICAL MEDICINE FOR NURSES. 


The heart action is very rapid (120 or more), respira¬ 
tion is rapid (usually above 30 to the minute), and usu¬ 
ally some cyanosis is present. There is no leukocytosis, 
this fact being an important element in diagnosis. 

The course of the disease is rapidly progressive, and 
the outcome invariably fatal. There is no treatment that 
is of any avail. 

Pulmonary tuberculosis. 

Clinical Varieties of Pulmonary Tuberculosis. These 
are three in number: 

(1) Acute miliary tuberculosis of the lungs. 

(2) Acute tuberculous pneumonia. 

(3) Chronic tuberculosis. 

1. Acute Miliary Tuberculosis of the Lungs. This 
form of tuberculosis occurs either 

(1) As a primary affection. 

(2) As a result of dissemination from a pre-exist¬ 

ing recognized or unsuspected focus of dis¬ 
ease in the lung. 

In either case, a large number of bacilli are suddenly 
set free in the lesser (pulmonary) circulation, so that 
the pulmonary tissue is bathed in blood rich in virulent 
tubercle bacilli. The result is the fonnation at approxi¬ 
mately one and the same time of an infinite number of 
miliary tubercles throughout the lungs. The tubercles 
are all young, and have the characteristic pearly-gray ap¬ 
pearance. Upon touching a lung filled with miliary 
tubercles, the sensation is exactly as though the lung 
were filled with bird-shot. 

Symptoms. These resemble very greatly those of 
acute general miliary tuberculosis, and therefore will not 


TUBERCULOSIS. 


195 


be repeated. Stress must be laid, however, upon two 
symptoms: 

(1) Dyspnea, 

(2) Slight cyanosis, 

which are practically the only ones that point to the lungs. 
Most of these patients have no cough, and few of them 
show expectoration. This form of tuberculosis of the 
lungs is uniformly fatal. A few cases are cited where 
the disease has changed into a more chronic type, and 
where life has been somewhat prolonged, but as a rule 
death ensues in from six weeks to three months. 

The treatment of this type of the disease differs in 
no way fromi the management of the ordinary bed case 
of subacute or chronic phthisis, and consequently will not 
be dealt with separately. 

2. Acute Tuberculous Pneumonia. In this type of pul¬ 
monary tuberculosis an entire lobe of the lung is involved. 
The picture at first is almost exactly similar to 
that of acute lobar pneumonia (q.v.), and in fact can 
with difficulty be distinguished from that disease, unless 
the patient is known to be tuberculous. There is the 
same high temperature, cough, sputum, pain in the side 
from pleurisy, dyspnea, and, in very severe cases, cya¬ 
nosis. Two points worthy of notice are that in acute 
pneumonia phthisis the sputum is rarely rusty , and that 
there is no leukocytosis. The affected lobe of the lung 
is solid (consolidated), as in lobar pneumonia. As time 
goes on, however, the picture changes. The expected 
crisis does not occur; instead, the temperature remains 
high, the patient becomes more and more toxic, the 
sputum becomes yellow, green, and mucopurulent, and, 
if the tubercles in the lungs have had time to caseate and 
break down, tubercle bacilli may be found in the sputum. 


196 


CLINICAL MEDICINE FOR NURSES. 


The course of the disease is either short or protracted. 
The writer has seen death occur within fourteen days 
from the onset of the disease, but in many cases the acute 
stage is weathered, and the disease goes over into the 
type of subacute or chronic ulcerative phthisis with ex¬ 
tensive cavity formation. In some cases recovery ensues; 
others that have been able to live through the most acute 
stage go on to a life of total or semi-invalidism for 
months or years. 

As in the case of acute miliary tuberculosis of the lungs, 
the management of these cases differs in no wise from 
that of bed cases of subacute or chronic phthisis, and will 
therefore not be dealt with here. 

3. Chronic Tuberculosis. This form of tuberculosis 
is by far the most common. It is divided into three 
classes: 

(a) Incipient. 

( b ) Moderately advanced. 

(c) Far advanced. 

An entirely satisfactory classification of pulmonary 
tuberculosis has not yet been reached. Attempts have 
been made to classify the disease according to the 
amount of involvement found in the lungs, and accord¬ 
ing to the symptoms presented by the patient. The best 
classification known to the writer is a combination of 
these two, which was adopted by the American Sana¬ 
toria Association. Though, strictly speaking, a classi¬ 
fication of pulmonary tuberculosis has nothing to do 
with the duties of the trained nurse, this classification is 
given, as it can, if carefully studied, give an insight 
into the many ways in which this disease may present 
itself. 


TUBERCULOSIS. 


197 


Lesions. 

Incipient. Slight infiltration 
limited to the apex of one or 
both lungs, or a small part of 
one lobe. No tuberculous 
complications. 

Moderately Advanced. Marked 
infiltration, more extensive 
than under incipient, with lit¬ 
tle or no evidence of cavity 
formation. No serious tuber¬ 
culous complications. 

Far Advanced. Extensive loc¬ 
alized infiltration or consoli¬ 
dation in . one or more lobes. 
Or disseminated areas of 
cavity formation. Or serious 
tuberculous complications. 


Symptoms. 

A. (Slight or none). Slight 
or no constitutional symp¬ 
toms, including, particularly, 
gastric or intestinal disturb¬ 
ance, or rapid loss of weight; 
slight elevation of tempera¬ 
ture or acceleration of pulse 
at any time during the 
twenty-four hours. Expec¬ 
toration usually small in 
amount or absent. Tuber¬ 
cle bacilli may be present or 
absent. 

B. (Moderate). No marked 
impairment of function, 
either local or constitutional. 

C. (Severe). Marked impair¬ 
ment of function, local and 
constitutional. 


This scheme is flexible in that it offers the following 
combinations: 

Incipient A. Moderately Advanced A. Far advanced A. 

Incipient B. Moderately Advanced B. Far Advanced B. 

Incipient C. Moderately Advanced C. Far Advanced C. 

Thus combinations of the local conditions in the lungs 
and of the general symptoms can be obtained which go 
far toward placing each individual case in its proper 
grouping. 

Symptoms. 

(a) Incipient. While the trained nurse will but very 
rarely be called upon to care for a case of really incipient 
tuberculosis, she should nevertheless be familiar with the 
symptoms of this condition, as it is only by spreading 
their characteristics and their importance throughout 
every community that the disease can ever be stamped out. 


198 


CLINICAL MEDICINE FOR NURSES. 


The symptoms of incipient pulmonary tuberculosis are 
vague and elusive. No one symptom is conclusive; all 
are but very rarely present; but the combination of any 
three or four are extremely suggestive. 

X. Not pointing to the lungs: 

(1) Fatigue. A loss of vigor and of ambition, a 

tired feeling out of proportion to the amount 
of work bringing it about, and from which 
the patient does not promptly recover. 

(2) Rapid heart action. Over 85 to 90, especially 

early in the morning, before arising. 

(3) Gradual and persistent loss of weight and 

strength. 

(4) Marked and unaccountable nervousness and 

irritability. 

(5) Loss of appetite and symptoms of indigestion. 

(6) Slight afternoon fever—99° to 99.5°—increased 

by moderate exertion, such as an hour’s walk. 

Y. Pointing to the lungs: 

(7) Cough. Slight, dry, hacking, most noticeable 

in the early morning. 

(8) Sputum. Grayish-white or light-yellow. Slight 

in amount, usually not exceeding 2 teaspoon¬ 
fuls in twenty-four hours. 

(9) Dyspnea. Usually slight, transient, and only 

noticed after some mild physical exertion. 

(10) Hemoptysis. 

( b) Moderately Advanced. The difference in the 
symptoms of an incipient and of a moderately advanced 
case is usually one of degree only. The strength of the 
patient becomes so poor that work is abandoned. The 
pulse-rate may or may not show a change. The weight 


TUBERCULOSIS. 


199 


is decidedly below par, and the emaciation of the patient 
becomes apparent. The temperature is more marked, 
rising usually from 100° to 101° in the afternoon, and 
often registering 98.6° to 99° in the morning. The cough 
becomes increasingly troublesome, and often disturbs the 
patient’s rest. It frequently assumes a looser and more 
hollow character, and may come on in such paroxysms as 
to cause vomiting. The sputum becomes more profuse, 
frequently reaching a total of 2 ounces in twenty-four 
hours, and, though there are many exceptions to this 
rule, generally becomes yellow, mucopurulent, and 
tenacious. Tubercle bacilli are usually present in the 
sputum. Dyspnea is more marked on exertion, and may 
even persist when the patient is at rest. Hemoptysis is 
more frequent than in the incipient stage, and, when it 
occurs, is apt to be more profuse. Night-sweats may 
put in their appearance, and tuberculous complications, 
especially tuberculosis of the larynx, are frequent. Dis¬ 
orders of digestion are more frequent and less tractable 
than in the incipient form. 

(c) Far Advanced. Here, again, the difference in 
symptoms between moderately advanced and far ad¬ 
vanced cases is one of degree only. The weakness and 
emaciation become extreme, and the patient is often ab¬ 
solutely bedridden. The pulse is usually over 100, and 
weak. The appetite is bad, and digestion is poor, these 
patients being greatly distressed by the copious forma¬ 
tion of gas in the intestines. The temperature may range 
from 99° to 103° or more, or else may be typically “sep¬ 
tic” in type, rising and falling with no reference to the 
time of day. Chills, especially in the morning, are fre¬ 
quent, and the nights are rendered hideous by the drench¬ 
ing sweats. Cough is severe, at times almost constant, 


200 


CLINICAL MEDICINE FOR NURSES. 


deep and hollow, and usually causes the patient to 
awaken a half-dozen times during the night. The spu¬ 
tum is copious, from 3 to 8 ounces in the twenty-four 
hours, yellow, or yellow-green, tenacious, often with a 
sweetish, sickening taste, and at times foul-smelling. 
Dyspnea is marked, constant, and is greatly increased by 
the slightest physical exertion. Hemoptysis is frequent, 
and when it occurs in any large amount is very serious 
and sometimes fatal. Tuberculous laryngitis, tuber¬ 
culous enteritis, and tuberculous meningitis are of fre¬ 
quent occurrence, especially the first two. Often, pa¬ 
tients can lie in but one position, usually on the rela¬ 
tively sound side, any change bringing on an exhausting 
fit of coughing. With the wretchedness incident to the 
high temperature, the cough, the sweats, the inability to 
eat, the frequent and painful complications, these unfor¬ 
tunates form one of the saddest sights in medicine, and 
many of them, fully aware of the helplessness of their 
condition, welcome death as a blessed deliverance. 

Modes of death in pulmonary tuberculosis. 

1. Exhaustion. By far the most frequent. 

2. Hemorrhage. Usually only in advanced cases with 
large cavity formation. 

3. Suffocation. Lung involvement so great that the 

remaining breathing-space is insufficient to main¬ 
tain life. 

4. Pulmonary edema. Sudden, and often the result 

of unexpected heart failure. 

5. Tuberculous laryngitis. Because of the relative 

starvation caused by the extreme pain on taking 
food, and by the regurgitation of food through 
the nose. 


TUBERCULOSIS. 


201 


6. Tuberculous enteritis. Because of the depleting 

effect of the prolonged diarrhea, and because of 
inability to digest or assimilate what little food 
can be taken. 

7. Tuberculous meningitis. Because of the dullness, 

stupor, and coma that ensue, making feeding al¬ 
most impossible, because of the practically abso¬ 
lute constipation, and because of the spread of 
the tuberculous poison throughout the central 
nervous system. 

Important complications of pulmonary tuberculosis. 

1. Hemoptysis (hemorrhage from the lungs). Hemop¬ 
tysis is very frequent, occurring to a greater or less ex¬ 
tent in about 60 per cent, of patients. The hemorrhage 
may be of any size, from a teaspoonful to 2 quarts. It 
may be preceded by the expectoration of blood-streaked 
sputum, but more often it occurs suddenly and unex¬ 
pectedly. Hemoptysis is caused by the eating away or 
erosion by the tuberculous process of one of the pul¬ 
monary vessels. If the vessel is small, the hemorrhage is 
usually slight; if the vessel is large— e.g., an artery run¬ 
ning across a cavity—the hemorrhage may be so great 
as to prove immediately fatal. Hemorrhages may occur 
singly, or several may follow one upon the other. At 
times, a hemorrhage may be directly traceable to some 
indiscretion—lifting, running, etc. More often, the ex¬ 
citing cause remains unknown. 

Symptoms. Frequently there are none until the pa¬ 
tient expectorates a mouthful of blood. At other times 
a tickling sensation is felt under the sternum, a warm, 
salty taste appears in the mouth, and blood is expector¬ 
ated. The blood is usually bright red and frothy. It 
may come only on cough, which is apt to be very fre- 


202 


CLINICAL MEDICINE FOR NURSES. 


quent, it may come so fast as to almost choke the patient, 
or, in extreme cases, it may pour from the patient’s mouth 
like Welter from a faucet. Later, blood is almost invari¬ 
ably vomited, as all is never expectorated, and some al¬ 
ways trickles down the esophagus into the stomach. After 
a fair-sized hemorrhage, patients almost always run a 
higher temperature for a few days, due to the absorption 
of the blood that has remained in the lung. If large cav¬ 
ities are present, the patient may suffer a severe loss of 
blood and expectorate but little, the main portion of blood 
lost being retained in the cavity. 

Dangers of hemorrhage: 

(a) Loss of blood. 

(b) Aspiration pneumonia. 

(c) Dissemination of tuberculous process. 

But a small percentage of patients that bleed actually 
die from loss of blood. Occasionally a bronchopneumonia 
sets in, usually of tuberculous origin, from which recovery 
is rather the rule than the exception. If, as a result of 
hemorrhage, as not infrequently happens, a spread occurs 
in the area of disease in the lung, its extent and character 
will determine the fate of the patient. 

2. Tuberculous Laryngitis. When we consider that 
every bit of germ-laden sputum that is expectorated passes 
through the larynx, the wonder is that cases of tuberculous 
laryngitis are not more frequent, but this is explained by 
the fact that the tubercle bacilli are imprisoned in tenacious 
mucus and therefore cannot easily find lodgment on the 
laryngeal tissues. The complication is, however, of very 
common occurrence. The first symptom may be any of 
the following: 

(a) Weakness and rapid fatigue of the voice. 

(b) Hoarseness in varying degree. 

(c) Pain in the throat, usually on swallowing. 


TUBERCULOSIS. 


203 


The amount of hoarseness and pain depend upon the 
extent of the process, and also upon the particular part 
of the larynx involved. Thus, a very slight involvement 
of the vocal cords will cause marked hoarseness, and 
sometimes complete aphonia, while far greater involve¬ 
ment of other structures of the larynx will affect the 
voice slightly, if at all. 

Where the epiglottis is involved there is very great 
pain on swallowing food, and food or fluid taken not in¬ 
frequently regurgitates through the nose. At times the 
pain radiates to the ears. In advanced cases an enormous 
quantity of mucus is secreted, which has to be expec¬ 
torated almost constantly, this serving to greatly exhaust 
the patient. In certain types of laryngeal tuberculosis the 
pain on trying to swallow food is so great that the pa¬ 
tient literally prefers to starve to death. 

3. Intestinal Tuberculosis (tuberculous enteritis). 
This condition may be primary— i.e., the beginning of 
active tuberculosis in the affected individual. Usually, 
however, it is secondary to advanced pulmonary disease. 
It is not an uncommon complication, and is very serious 
indeed, practically all cases going steadily downhill. 
Ulceration occurs in the large and small intestine. 
Hemorrhage from the ulcers may occur, though this is 
rare as compared with hemorrhage from typhoid ulcers, 
because of the nature of the tuberculous process, which 
tends to block up and shut off the blood supply from the 
invaded area. Tuberculous ulcers have their long axis 
around the intestine, in contrast to typhoid ulcers, whose 
long axis runs lengthwise to the intestine. 

Persistent and repeated digestive complaints, a feeling 
of fulness in the abdomen, the belching of gas and the 
passing of flatus, failure to assimilate food and to gain 


204 


CLINICAL MEDICINE FOR NURSES. 


weight; all these form a picture which should lead to a 
suspicion of the presence of tuberculous enteritis. The 
main symptom, however, of intestinal tuberculosis is an 
obstinate, intractable, painful diarrhea, sometimes alter¬ 
nating with periods of constipation, the stools number¬ 
ing from 4 to 12 per day, and having a rather character¬ 
istic and extremely offensive odor. With this diarrhea 
there is profuse gas formation, almost constant abdom¬ 
inal pain, a distaste for food, and marked and progressive 
emaciation. Death usually occurs from exhaustion. 

4. Tuberculous Meningitis. This complication, though 
not as common in adults as the three preceding ones, is 
not infrequently met with. It is extremely fatal, many 
authorities placing the mortality at 100 per cent. There 
are no absolutely characteristic symptoms of tuberculous 
meningitis that serve to differentiate it from any other 
meningitis, save the examination of the spinal fluid (see 
section on Lumbar Puncture in chapter on Epidemic 
Cerebrospinal Meningitis) and the finding therein of 
tubercle bacilli. 

When, however, a tuberculous patient presents the 
three following symptoms, the existence of a tuberculous 
meningitis becomes practically a certainty: 

(a) Headache. Marked, persistent, becoming grad¬ 

ually worse. Resistant to all manner of treat¬ 
ment. 

(b) Vomiting. Constant, not associated with the 

taking of food. 

( c ) Constipation. Marked, and growing progres¬ 

sively worse. Short of absolute intestinal ob¬ 
struction, there is no more: marked constipation 
than that found in tuberculous meningitis. 

In addition there are present symptoms of meningitis 
in general—at first those of cerebral irritation, and later 


TUBERCULOSIS. 


205 


those of cerebral depression. (See chapter on Epidemic 
Cerebrospinal Meningitis). Patients die from exhaus¬ 
tion, starvation; from absorption of toxins from the 
bowels; and from the spread of the tuberculous process 
throughout the central nervous system. 

Prophylaxis. The prevention of tuberculosis is the 
cornerstone upon which is erected the hope for the 
future eradication of the disease. Prophylaxis may be 
divided into four classes: 

(1) National. 

(2) State. 

(3) Municipal. 

(4) Individual. 

National and state prophylaxis do not come within the 
scope of these lectures. Municipal prophylaxis also will 
not be considered in detail, but the following list will 
serve to show the different paths by which control and 
prevention of the disease is being sought: 

(a) Report to the local board of health of all cases 

of tuberculosis. 

(b) Tuberculosis clinics. 

(c) Tuberculosis classes. 

( d ) Day camps for the tuberculous. 

( e ) Night camps for the tuberculous. 

(/) Sanatoria. 

(1) For incipient cases. 

(2) For advanced cases. 

(g) Public lectures, free of charge. 

( h ) Public exhibits, free of charge. 

(i) Posters illustrating preventive measures. 

(/) Instruction leaflets widely circulated, free of 
charge. 

( k ) District tuberculosis nurses to visit the homes 
of the tuberculous poor, free of charge. 


206 CLINICAL MEDICINE FOR NURSES. 

(/) Providing, free of charge, the few necessaries to 
make the tuberculous individual no longer a 
source of danger, and to enable him to take 
rational care of himself—sputum cup, ther¬ 
mometers, disinfectants, etc. 

Individual Prophylaxis. This subdivision will be dis¬ 
cussed more in detail, as the nurse must see that the 
necessary precautions are scrupulously carried out, both 
for her own protection and for that of the members of 
the family of her patient. 

(a) Care of the Sputum. It is probable that at the end 
of fifty, years “if all sputum were destroyed there would 
be no tuberculosis,” for the germ-laden sputum is by 
far the most important agency in spreading the disease. 
Every patient having sputum, whether bacilli have been 
found in it or not, should possess a sputum-box, and 
invariably expectorate in that box. The best box is one 
consisting of a tin holder into which paper fillers are 
fitted. Every twenty-four hours the filler (whether full 
or not) is removed from the holder and burned with its 
contents. Very finicky patients will not, and very weak 
patients often can not, use a sputum-box. For such pa¬ 
tients the nurse should provide small squares of cheese¬ 
cloth, gauze, or tissue paper into which the sputum can 
be expectorated. An ordinary paper bag pinned to the 
sheet within easy reach of the patient serves as a re¬ 
ceptacle for these cloths, and every twelve hours the bag 
and its contents should be burned. 

(h) Covering the Mouth when Coughing. The nurse 
should provide a liberal number of gauze or cheesecloth 
squares for this purpose, as it has been shown that in 
the act of coughing minute particles of sputum contain¬ 
ing bacilli may be expectorated. A nurse should insist 
upon the patient observing this rule, which is the one 


TUBERCULOSIS. 


207 


above all others that even conscientious patients are prone 
to neglect. 

(c) Separate Dishes and Table Utensils. The patient 
should use separate dishes from the rest of the family. 
It is well for the nurse to suggest that these dishes be 
of a different pattern. Silverware (knives, forks, and 
spoons), napkins and tray-cloths should not be mixed with 
the family supply. Paper napkins are desirable, as they 
can be burnt. 

( d ) Frequent Hand-washing. The patient should 
wash the hands frequently, especially before and after 
meals, and should repeatedly rinse the mouth with some 
mildly antiseptic mouth wash, such as Dobell’s solution. 

(e) Bedclothing and Bedlinen. These should be dealt 
with separately from the family washing, and should be 
thoroughly boiled. 

(/) Care of Thermometers, etc. All thermometers 
should be kept in a bichloride (1:1000) or carbolic (5 
per cent.) solution, and washed with water before being 
given to the patient. Rectal tubes, enema nozzles, etc., 
should be sterilized after use by boiling. 

(g) The Nurse's Care of Herself. The nurse should 
insist upon a reasonable amount of time off duty, should 
take a daily brisk walk of at least half an hour, should 
pay scrupulous attention to the care of her hands and 
mouth, and should never use any article that has been 
used by the patient. 

By rigid adherence to the few simple rules here given, 
the patient will prove absolutely no danger to the house¬ 
hold in which he lives, and the nurse will be doing, in 
addition to her professional duty, an educational work 
in the family and in the community in which she is called 
upon to practice. 


208 


CLINICAL MEDICINE FOR NURSES. 


Treatment. The treatment of tuberculosis may be 
divided into four groups: 

(1) Hygienic-dietetic treatment. By far the most 

important. 

(2) Specific treatment, i.e., tuberculin. In con- 

(3) Treatment by the induction of ar- >■ junction 

tificial pneumothorax. ) with 1. 

(4) Symptomatic treatment. 

Hygienic-dietetic Treatment . This is based on three 

equally important factors: 

(x) Rest. 

(y) Fresh air. 

(s) Food. 

The nurse will so rarely be called upon to care for the 
case that is truly ambulant that it is not necessary to go 
into the details of the regime. A few general rules will 
merely be laid down without comment: 

(1) Rest at first, and until exercise is ordered. 

(2) Day spent on porch in reclining chair. 

(3) Temperature and pulse taken four times daily 

and oftener at first. 

(4) Three full meals per day, at the usual hours, 

supplemented by such additional nourishment 

as ordered. 

(5) Exercise when ordered, and in the amount 

prescribed. 

(6) Sleep on porch or in room with all windows 

open. 

(7) In bed not later than 10 p.m. 

(8) Drugs only for combating individual symptoms. 

(9) No alcohol in any form. 

Bed Cases. The vast majority of cases of pulmonary 
tuberculosis employing a trained nurse are bed cases at 
the time of the nurse’s arrival. As a typical example will 
be selected a moderately advanced case, running a maxi¬ 
mum daily temperature between 101° to 102°, with other 
symptoms in proportion. 


TUBERCULOSIS. 


209 


I. General Management. If the patient has a sleeping 
porch it will, of course, be used. See that the bed is in a 
protected portion of the porch, and that the patient is 
not liable to be wet by a driving rain. If necessary, ask 
for an awning or a canvas shield for the exposed end of 
the porch. If there is no sleeping porch available, the 
room must be as freely open to the air as possible. Cold, 
rain, etc., are no contraindications to this, it being of 
course understood that the patient is to be at all times 
warm and comfortable. The head of the bed should not 
be in a corner where there is air stagnation, nor between 
two windows where a direct draught blows on the patient, 
but well out in the body of the room where air circulates 
freely. Sacrifice the looks of the room to the welfare 
of the patient. In winter the nurse must be sure to 
provide herself with warm clothes, both under and outer 
garments, in order that she, too, will be comfortable in 
cold weather. The writer has known of several nurses 
rendered seriously ill by the combination of insufficient 
clothing and devotion to their patients. The nurse owes 
her services to her patient, but she owes her health to 
herself; it is her most precious asset. 

Save in conditions of great weakness, or after hemor¬ 
rhage, the bedpan is usually not necessary. If the bath¬ 
room is convenient, it can be used, or else recourse can 
be had to a commode. 

Care must be taken not to expose the patient in cold 
weather. If a porch is used, he must be rolled into the 
room for the morning toilet, which differs in no way 
from that of any case of febrile disease—bath, rub, etc. 
If the patient is in a room, it must be warm before any 
work is undertaken with the patient. This is excessively 
important, and often neglected. 

14 


210 


CLINICAL MEDICINE FOR NURSES. 


II. Food. Tuberculosis being a wasting disease, food 
is excessively important. The normal caloric needs of 
the body must be exceeded, for oxydation of foodstuffs 
and of tissues is going on more rapidly than in the nor¬ 
mal individual. There are no absolute rules for diet in 
tuberculosis. There is no one diet in tuberculosis. Gen¬ 
erally speaking, the caloric needs of the patient will be 
supplied by “three square meals a day and a little more/’ 
the “little more” coming in the form usually of eggs 
and milk, to be taken as prescribed by the physician. 

Certain general principles of diet will be mentioned. 
The application of accurate caloric feeding is rarely 
practiced, save in an institution under the super¬ 
vision of a dietician assisted by several nurses. In the 
ordinary case encountered in private nursing a general 
estimate of the caloric value of food taken will be made, 
and feeding directed upon that as a basis. 

Food for the tuberculous should be well prepared— 
cleanly, promptly, and attractively served. The ordinary 
articles of diet are satisfactory. Meat should not, as a 
rule, be eaten more than once a day. It is not wise to 
increase too greatly the proteid intake. For the sake of 
gaining weight, carbohydrates and fats should be in¬ 
creased more than the nitrogenous food. Extra nourish¬ 
ment is usually indicated in the majority of cases. The 
simplest way to give it is in the form of milk and eggs. 
Fortunately, the days of tremendous overfeeding are 
past, and now the object is to give just as much as the 
stomach will tolerate, but no more. 

Many tuberculous patients, especially those running 
some temperature, have poor appetites, and a consider¬ 
able part of the nurse’s duty will be to try and make 
these patients eat. The few suggestions on the prepara- 


TUBERCULOSIS. 


211 


tion and serving of food for the sick in the chapter on 
“Foods and Nutrition” apply particularly well to tuber¬ 
culosis. Many patients announce at once: “I cannot 
take milk and eggs.” As a matter of fact, this usually 
means: “I dislike milk and eggs, and I don't want to 
take them.” 

There are some patients that really cannot take milk 
and eggs, every attempt so to do causing marked symp¬ 
toms of indigestion. These patients are greatly handi¬ 
capped, but fortunately their number is small. As a 
rule, by coaxing, by disguising the taste of the milk with 
very little tea or coffee, by beating up the egg in the 
milk and adding a little vanilla, by having milk and egg 
ice cold, by beginning with the white of the egg and not 
adding the yolk until later, or by many other little sub¬ 
terfuges, the patient, if really in earnest and co-opera¬ 
tive, can manage to take eggs and milk. 

Too much care and attention cannot be expended by 
the nurse on the patient’s food. The tripod upon which 
rests the treatment of tuberculosis is: rest, fresh air, 
food. Rest can be obtained; fresh air is within the reach 
of all; but food not only must be well selected but well 
cooked, and served in such a manner as to overcome 
aversion on the part of a stomach that instinctively re¬ 
volts at the thought of a meal. 

III. Bowels. The care of the bowels is extremely im¬ 
portant. Save in those cases of tuberculous enteritis, or 
during some transitory intestinal derangement, constipa¬ 
tion is the rule. It is very natural that this should be so, 
for the patient is put to bed, allowed no exercise whatso¬ 
ever, and fed very liberally. Many of the cases of con¬ 
stipation clear up in a marked degree when the patient 
is able to take thirty minutes’ exercise. Laxatives must 


212 


CLINICAL MEDICINE FOR NURSES. 


be resorted to in the majority of cases. As a general 
rule, it can be stated that it is better for the patient to 
have two bowel movements daily than to go one day 
without a thorough evacuation. 

IV. Cough. There is no symptom more wearing and 
exhausting than cough, and many bed-patients are act¬ 
ually greatly overexercising as a result of the exertions 
incident to the cough. There are, generally speaking, 
two kinds of cough in pulmonary tuberculosis: 

(1) Dry—hacking—bringing up no sputum. This 

cough, like that in the beginning of lobar 
pneumonia, is “never helpful, always trouble¬ 
some, sometimes dangerous/’ and should be 
discouraged. About 75 per cent, of it can 
be controlled by the will. The nurse should 
keep this before the patient, and gradually 
she will see the fruits of her suggestion in 
lessened hacking, more rest, and increasing 
strength. At times, cold cloths or an ice-bag 
to the throat is of great value in relieving the 
dry, harassing cough. Almost invariably, 
some drugs are necessary to help the cough, 
an opium derivative, like codeine or heroin 
being usually the cornerstone of the pre¬ 
scription. 

(2) Loose, productive cough, bringing up sputum. 

This type of cough is beneficial. It is 
Nature’s method of drainage, and should not 
be interfered with. 

V. Temperature. Rest in bed is the best treatment for 
fever. Moderate temperatures, up to 103°, rarely re¬ 
quire any active treatment other than bed-rest. With 
higher temperatures, cold, in the form of the ice-cap, 


TUBERCULOSIS. 


213 


gives relief, as do also sponges with alcohol and water. 
With very high fever, or in patients that feel very badly 
indeed with a moderate amount of temperature, anti¬ 
pyretics are used. 

VI. Night-sweats. As night-sweats are simply a 
symptom of toxemia, that which reduces the toxemia 
will also cause the disappearance of the sweats. Rest 
in bed is the best treatment for night-sweats, as it re¬ 
moves, or at any rate lessens, the cause. Drugs are also 
of value for night-sweats, several being used, the most 
reliable being atropin and camphoric acid. Alcohol and 
vinegar rubs at night are also sometimes of benefit. 

VII. Insomnia. Often very intractable. The success 
of its management depends almost entirely upon the 
underlying cause. If cough is the cause, its alleviation 
will be of great benefit. For the sleeplessness apparently 
without cause that so often troubles tuberculous patients, 
but little is to be done. The condition is probably an ex¬ 
pression of toxemia, and rest in bed is the best treat¬ 
ment. Practically all physicians hesitate to give hyp¬ 
notics in these cases because of the great dependence so 
soon placed upon them, but often it is absolutely neces¬ 
sary to employ them for a short while. 

VIII. Vomiting. There are two kinds of vomiting 
seen in tuberculosis: 

(1) Vomiting due to local stomach conditions. The 
digestive system is then at fault and treatment must be 
directed toward the correction of whatever is out of 
gear. 

(2) Vomiting due to coughing, and of purely mechani¬ 
cal origin, there being no disturbance whatsoever of the 
gastro-intestinal tract. This vomiting is particularly 
marked during or after breakfast. The warm food and 


214 


CLINICAL MEDICINE FOR NURSES. 


coffee taken at breakfast serve to loosen the secretions 
in the lungs. These cause cough in order that expectora¬ 
tion may take place. The diaphragm pressing down 
with each cough upon the recently filled stomach, finally 
causes a gastric contraction which results in vomiting. 
These cases can often be very well dealt with by giving 
the patient a glass of hot water on awakening. The 
water is to be sipped slowly. It acts as a “loosener” to 
the secretions, and coughing and expectoration take place 
before breakfast, and on an empty rather than on a full 
stomach. 

Management of important complications. 

1. Hemorrhage. The following facts must be plainly 
understood with regard to pulmonary hemorrhage: 

(1) Hemorrhages are largely self-limited. 

(2) No treatment by drugs for rapidly stopping 

hemorrhage is of much avail unless instituted 
within five minutes after bleeding has begun. 

(3) Certain symptoms that make for more free 

bleeding can be satisfactorily controlled by 
drugs. 

(4) The mental attitude of the patient during a 

hemorrhage is as important as anything con¬ 
nected with the treatment of the condition. 

(5) The attitude of the nurse in an emergency such 

as hemorrhage will largely determine the 
attitude of the patient. 

The patient, with very few exceptions, is badly fright¬ 
ened. The nurse must keep her head, be calm, take 
charge of things, and convey the impression that bleed¬ 
ing is nothing over which to be alarmed. Her place is 
with her patient—not calling up half-a-dozen telephone 


TUBERCULOSIS. 


215 


numbers in vain attempts to locate the physician. That 
important duty should be delegated to someone else. 

That we have no specific for pulmonary hemorrhage 
is shown by the fact that almost every drug in the phar¬ 
macopeia has been used at some time or other. This, too, 
is a strong argument in favor of the self-limiting nature of 
pulmonary hemorrhage. A brief statement of the general 
management of hemoptysis, and a few words concerning 
some of the most used methods will suffice. 

The patient that is bleeding should at once be put to 
bed, if not already there; one pillow under the head (some 
authorities preferring an almost erect position), small 
amounts of salt and cracked ice by mouth. The patient 
should not be allowed to raise himself on his elbow to 
expectorate into the sputum cup. Sputum should be re¬ 
ceived into cloths—gauze, towels—anything that is at 
hand, and as far as possible the position of the patient 
should not be disturbed. 

As to drug treatment, morphia is very often and very 
freely given—sometimes too freely. Morphia is, of course, 
the great dnig for allaying intense nervousness and un¬ 
controllable cough, and in a large percentage of cases 
will be indicated and required. For frequent dis¬ 
tressing cough, codein acts very well, being given 
hypodermically. The drug that has given the author 
the best results in the control of bleeding is atropine, V33 
to y 2 5 grain hypodermically. The dose is large, but the 
effect is to reduce deep blood-pressure by the dilation of 
the superficial vessels all over the body. The results are 
prompt, if administered at once upon the appearance of 
free bleeding but are nil if delayed. An amyl nitrite 
pearl is frequently given the patient while the hypoder¬ 
mic is being prepared. 


216 


CLINICAL MEDICINE FOR NURSES. 


The calcium salts are frequently used in hemorrhage 
cases, because of their action in increasing the coagula¬ 
bility of the blood. The chloride and lactate of calcium 
are the salts employed. The writer has seen good results 
from the administration of coagulose. 

During and after a hemorrhage, the patient should be 
kept in that position which is found to be most comfort¬ 
able and securing the greatest bodily relaxation. Some 
patients prefer to be propped up, others to lie flat, still 
others to lie on one side. Absolute quiet with use of bed- 
pan and urinal must be insisted upon until the sputum is 
clear of blood. For several days after active bleeding 
there is sure to be red sputum, and the nurse must re¬ 
assure the patient that this does not signify renewal of 
bleeding. 

For twenty-four hours after a smart hemorrhage nour¬ 
ishment should be liquid, and nothing hot should be given 
until the sputum is again clear. Attention must be given 
to keeping the bowels well open by laxatives or enemata. 

2 . Pleurisy. This subject is dealt with in the chapter 
on “Pleurisy—Dry and with Effusion,” and therefore will 
not be discussed here. 

3. Tuberculous laryngitis. The actual treatment of 
tuberculous laryngitis falls outside the province of the 
nurse. There are a few things, however, that she can do 
for patients with this complication: 

(a) Spraying the throat. Sprays or powders, both 
for .treatment and as anesthetics, are often 
prescribed, and rarely satisfactorily admin¬ 
istered. A spray or powder improperly given 
is worse than no spray at all. Hence, the fol¬ 
lowing directions for spraying the larynx are 
given: 


TUBERCULOSIS. 


217 


(1) Turn adjustable tip of atomizer downward 

until it makes an angle just short of a right- 
angle. 

(2) Let patient sit upright facing a good light, 

either natural or artificial. 

(3) Let patient pull out tongue as far as possible 

with a piece of gauze, and hold it thus. 
(This raises and immobilizes the larynx.) 

(4) Quickly insert barrel of atomizer into mouth, 

holding it in the median line, and having 
the tip about inch from the posterior 
pharyngeal wall. 

(5) Tell the patient to take a long, slow breath, 

and during that breath press bulb of 
atomizer vigorously three or four times. 

(6) As soon as patient begins to gag, withdraw 

atomizer, as its contents can no longer 
reach their goal. 

(7) Repeat this three or four times at the speci¬ 

fied hour at which the spray is used. 

(8) For the insufflation of powders the procedure 

is exactly the same, save that two good 
“puffs” of the powder are usually enough 
for one dose. 

( b ) Cold to the throat. This should be applied 

either by cold cloths constantly changed, or by 
means of the throat ice-bag, which adapts 
itself to the shape of the neck. The ordinary 
ice-bag or ice-cap is useless for this purpose. 

(c) Fly-blisters (cantharides plasters) are often 

used on the sides of the neck over the point 
of maximum laryngeal pain. 


218 


CLINICAL MEDICINE FOR NURSES. 


( d) Silence. If talking is prohibited, the nurse must 
see that silence is enforced. She must have 
paper and pencil at hand for the patient to 
write upon, and she must never answer any 
spoken question. 

4. Tuberculous Enteritis. This condition is usually one 
of the terminal phases of pulmonary tuberculosis. 
The intravenous injection of from 5 to 10 c.c. of a 5 
per cent, calcium chloride solution once or twice a week 
has often given excellent results in lessening diarrhea and 
relieving pain. Opium, in some form, must, however, be 
frequently resorted to. 

5. Tuberculous Meningitis. The treatment of this com¬ 
plication is purely symptomatic. At times, much relief 
can be obtained by frequent lumbar punctures, which, by 
lessening pressure in the spinal canal and in the ventricles 
of the brain, often causes great relief in symptoms, this 
relief being, unfortunately, only temporary. 

Tuberculin Treatment. It is not intended in these 
lectures to touch upon the question of treatment with 
tuberculin, for that rests wholly within the province of 
the physician. The following statements can be made, 
however. 

1. Tuberculin is any substance derived directly or in¬ 
directly from the tubercle bacillus and used therapeutically. 

2. There are over fifty varieties of tuberculin. 

3. The object of treatment with any tuberculin is to 
stimulate the body to the greater production of protective 
substances (antibodies) against the tubercle bacillus and 
its toxins— i.e., the bringing about of an active immunity 
to tuberculosis. 

4. There is no doubt that in certain cases tuberculin 
can be of inestimable value. 


TUBERCULOSIS. 


219 


5. There is no doubt that in the past tuberculin has 
been held up as a poison which it was criminal to use, 
and has been given credit for working miracles. Both 
extreme positions are unjustifiable. 

Treatment by the Induction of Artificial Pneumo¬ 
thorax. This mode of treatment, first devised by For- 
lanini, of the University of Pavia, Italy, in 1882, merits a 
short consideration. The object of artificial pneumo¬ 
thorax is to collapse and immobilize the affected lung by 
means of an “air splint,” and, as a result of this collapse 
and immobilization, to further healing and scar forma¬ 
tion by giving absolute rest to the diseased organ. 

In the small operation (which corresponds very much 
to tapping the chest for fluid) necessary for the induc¬ 
tion of artificial pneumothorax, a blunt, hollow needle is 
inserted between the ribs until its point is between the 
two pleural layers, this being indicated by certain charac¬ 
teristic fluctuations of a column of water in a U-tube, 
known as a manometer, which is connected by a tube 
with the needle in the chest. The point of the needle 
being in the desired position, the manometer is turned off 
and nitrogen gas or sterile air allowed to flow in. The 
gas spreads, of course, in the direction of least resist¬ 
ance. Toward the outside are the ribs and the firm in¬ 
tercostal muscles, forming an unyielding wall. Toward 
the inside is the soft, spongy lung, which gives way and 
shrinks much as does a sponge when squeezed. Grad¬ 
ually, after several injections, the lung is completely col¬ 
lapsed, the entire pleural cavity being filled with gas. 
When successful, the collapse of the diseased lung causes 
a prompt diminution in all symptoms, a lessening of 
fever, cough, sputum, a return of strength and well¬ 
being that in some cases is little short of miraculous. 


220 


CLINICAL MEDICINE FOR NURSES. 


Collapse is maintained for from six months to 
three years, and at the end of that time, healing having 
taken place, no more gas is given, and the lung slowly 
re-expands. 

Two factors are necessary for the induction of arti¬ 
ficial pneumothorax: 

1. One sound or almost sound lung, in order that it 
will, unaided, be able to carry on the task of respiration. 

2. Absence or scarcity of pleural adhesions. If ad¬ 
hesions between the two pleural layers are so dense that 
they will not give way under pressure from the gas, no 
collapse can be obtained and the procedure cannot be 
used. Failure occurs in about 33 per cent, of all attempts. 

Thus, taking the treatment of pulmonary tuberculosis 
and very briefly summarizing it, the following scheme 
can be presented: 

1. Hygienic-dietetic treatment. Applicable to every 
case. Based essentially on 

(a) Rest. 

( b ) Fresh air. 

(c) Food. 

2. Treatment with tuberculin. Applicable to a mod¬ 
erate number of cases. 

3. Treatment by means of artificial pneumothorax. 
Applicable to a very small percentage of cases (about 5 
per cent.). 

4. Symptomatic treatment. Very important, and, in 
conjunction with No. 1, applicable to every case. 


CHAPTER XXIII. 
SCARLET FEVER. 


Scarlet fever is an acute infectious disease having as 
its main features a characteristic rash, an inflamed and 
painful throat, and a high temperature, usually of short 
duration. One attack of scarlet fever usually confers 
immunity from further attacks, though this rule has occa¬ 
sional exceptions. It usually occurs before the tenth 
year, but infants are rarely attacked. 

The disease is very highly contagious, and is looked 
upon as being probably an infection with some form of 
streptococcus. The main sources of contagion are: 

1. The patient. 

2. The room occupied by the patient and its contents. 

3. A third person—nurse or doctor. This mode of 
contagion must be very rare, and is wholly denied by 
some authorities. 

The period of incubation is from 2 to 6 days. 

“ “ “ invasion “ “ 12 “ 24 hours. 

“ “ “ eruption “ “ 4 “ 6 days. 

“ “ “ desquamation “ “ 3 “ 6 weeks. 

Symptoms (average attack). The onset is sudden,, 
and often accompanied by vomiting. The temperature 
rises rapidly to 103° or 104°, with the usual symptoms of 
fever. There is redness of the pharynx and tonsils, and 
small red spots are seen on the hard palate. The red' 
ness of the throat is somewhat characteristic. It is a 
dark, deep crimson blush, quite uniformly spread over the 
entire pharynx and both tonsils. The tongue is known as 

(221) 


222 


CLINICAL MEDICINE FOR NURSES. 


the “strawberry” tongue, and is very well named. The 
papillae at the tip of the tongue are swollen, and the re¬ 
semblance to the rough surface of a strawberry is very 
marked. The glands of the neck are invariably swollen 
and tender. 

The rash develops in from twelve to thirty-six hours 
after the appearance of the first symptoms. It is first 
seen on the neck and chest, and gradually spreads over 
the entire body. The rash is what is known as a uniform 
diffuse erythema. On close examination it appears to be 
made up of countless minute red points. When de¬ 
veloped, it gives the impression of an evenly distributed 
blush, not distorting the countenance, as does the rash 
of measles. Unfortunately, the rash of scarlet fever 
often varies, both in character, intensity, and distribu¬ 
tion, and at times may be almost absent. Such cases, 
with very slight rash, are often unrecognized, and must 
be one of the important factors in furthering the spread 
of the disease. The rash lasts from three to seven days, 
when desquamation sets it. With subsidence of the rash 
the temperature gradually drops to normal. 

Desquamation in scarlet fever is a very long process, 
lasting from three to six weeks. Peeling takes place in 
the form of very fine scales, and is most apparent in 
those portions of the body where the skin is thickest— i.e., 
the palms of the hands and the soles of the feet. In these 
localities desquamation often occurs in large “sheets,” 
occasionally an entire “cast” of the palm of the hand 
or the sole of the foot being given off. 

In mild cases the temperature may not exceed 103°, and 
lasts from three to five days. In severe cases, the fever 
is higher and more continued, there is greater prostration, 
and all the signs of a severe general infection are marked. 


SCARLET FEVER. 


223 


Finally, there are the cases of so-called “malignant’’ scar¬ 
let fever, in which the patient is completely overwhelmed 
by the intensity of the infection, and death occurs in from 
twelve to seventy-two hours. 

Complications. 

1. Acute nephritis. Scarlet fever is one of the most 
common causes of acute nephritis. The symptoms of 
this condition are dwelt upon in detail in the proper 
chapter, but a few words must be said here concerning 
this dangerous complication. The nurse must remember 
that the two signs of a beginning nephritis in the course 
of scarlet fever are: 

(a) Edema. The child has a rather puffy look, 

especially noticeable in the face. 

( b ) Diminution in the amount of urine. 

Either one or both of these symptoms are of the utmost 
importance, and demand immediate notification of the 
physician. 

The nurse must also bear in mind two things in con¬ 
nection with scarlatinal nephritis: 

(1) The most severe nephritis may occur as a com¬ 

plication of the mildest attack of scarlet 

fever. 

(2) Acute nephritis very frequently occurs during 

convalescence from scarlet fever. 

In short, no nurse caring for a case of scarlet fever 
can lower her vigilance for the signs of a beginning 
nephritis until she is dismissed from the case. Usually, 
the patient’s condition during the long period of des¬ 
quamation is so satisfactory that daily visits on the part 
of the physician are not needful, when he is aided by 
the watchfulness of a competent and interested nurse. 


224 CLINICAL MEDICINE FOR NURSES. 

2. Acute otitis media. This is the most frequent 
complication of scarlet fever, but is not as dangerous as 
acute nephritis. If the otitis occurs at the height of the 
disease, there may be no symptoms. If during convales¬ 
cence, earache and a rise in temperature are characteris¬ 
tic. As a rule, both ears are involved at different times. 

3. A membranous inflammation of the larynx may 
occur, giving rise to symptoms similar to those observed 
in laryngeal diphtheria ( q.v .). 

4. Other infectious diseases, especially diphtheria, may 
complicate scarlet fever. 

Prognosis. The outlook in scarlet fever is always 
serious. The younger the child the graver the situation. 
Save for the malignant cases, scarlet fever, in the ab¬ 
sence of complications, is not a very fatal disease, but 
the frequent occurrence of dangerous complications 
makes it a malady to be dreaded. In mild types of the 
disease the mortality is under 5 per cent. In severe 
types, it may be as high as 50 per cent. 

Prophylaxis. The following directions for the estab¬ 
lishment of quarantine hold good for scarlet fever, 
measles, and diphtheria, varying only in the length of 
time quarantine is to be maintained. 

Room quarantine is to be installed at once, and main¬ 
tained for the time designated by the local board of 
health—as a rule, from four to six weeks. Nurse and 
patient are to be isolated in the sick-room. When pos¬ 
sible, a connecting bath is desirable, and, if practicable, 
a little diet kitchen should be installed in the bath-room, 
using a small gasoline or gas stove, so that no article 
need be sent out of the sick-room. In the vast majority 
of cases of scarlet fever, such conveniences will not be 
obtainable, and the best possible must then be done. 


SCARLET FEVER. 


225 


A sheet moistened with bichloride of mercury solution 
(1: 1000) or carbolic acid (5 per cent.) should be hung 
before the door. In the author’s opinion, this procedure 
has no great value in preventing the dissemination of 
infectious material, but the striking appearance of the 
sheet before the door has a wholesome effect upon mem¬ 
bers of the family inclined to carelessness, and acts ad¬ 
mirably as a “No Admittance” sign. 

All food brought to the sick-room should be left at 
the door, and taken in by the nurse. Before the dishes 
and other utensils are replaced outside the sick-room 
they should be allowed to soak for two hours in bi¬ 
chloride (1:1000) or carbolic (5 per cent.) solution. 
All bed linen, towels, gowns, etc., should be similarly 
treated before being set outside to be washed. Both 
dishes and bedclothes should not be washed in conjunc¬ 
tion with those used by the family. 

The room should be cleared of all unnecessary furni¬ 
ture, rugs, curtains, etc., and should be frequently cleaned 
by the nurse by being rubbed with a cloth wet with 
bichloride (1: 1000). 

The attending physician should have a gown and cap 
which he should put on every time he visits the patient. 
These should be hung on a hook just inside the door. 
If no gown and cap are available, a very satisfactory 
gown can be made from a sheet, and a small towel pinned 
“turban fashion” makes a thoroughly practical cap. The 
nurse should have at hand a basin with soap and water, 
a basin of bichloride solution, and a towel for the physi¬ 
cian at his visit. She should also request tongue de¬ 
pressors (wooden ones are the best), so that throat ex¬ 
aminations can be easily made, and recourse to the un¬ 
hygienic spoon become unnecessary. If the nurse will 

15 


226 


CLINICAL MEDICINE FOR NURSES. 


provide herself with a pocket flash-light, which she will 
find useful in many ways, she will often greatly aid the 
physician, who may have left his at home. 

At the termination of the period of quarantine the 
nurse should give her patient a bath in bichloride 
(1:5000), and wash the hair well with this solution. 
Following this, the patient should have an ordinary hot 
bath, and put on clothes that have not been in the sick¬ 
room. The nurse should then take her own bichloride 
bath, wash her hair, take a hot bath, and also put on 
clothes that have not been in the sick-room. 

Treatment. We have at our command absolutely no 
means of shortening or altering the course of scarlet 
fever, which is wholly a self-limited disease. Treat¬ 
ment is purely symptomatic. 

Bed, liquid diet during the period of fever, and keep¬ 
ing the bowels well open, are the foundation-stones for 
the management of a case of scarlet fever. During the 
eruption the patient should be anointed daily with vase¬ 
line or cocoa butter. After the rash has disappeared, 
daily warm baths with soap and water are frequently 
used. For very high temperature cold sponging gives 
the best results. When toxemia is very severe, stimu¬ 
lation may be necessary, according to the discretion of 
the physician in charge. It is usual to give a gargle or 
to prescribe some antiseptic with which the throat is to 
be swabbed. 

One of the essentials in nursing scarlet fever is eternal 
watchfulness for complications. During the long and 
tedious period of desquamation, when the child feels 
quite well, and must still remain isolated, the nurse will 
have to tax to their uttermost her talents for diverting 
and amusing her little patient. 


CHAPTER XXIV. 

MEASLES. 

Measles is. an epidemic contagious disease, and is 
more widespread than any other eruptive fever. 

Incubation, i.e., from date of exposure to onset 
of catarrhal symptoms, from eleven to fourteen 
days. 

Invasion, i.e., from onset of catarrhal symptoms to 
the development of the rash, usually three to 
four days. 

- Eruption, i.e., duration of the rash, four to six days. 

Desquamation, i.e., “peeling/’ one to two weeks. 

Etiology. The essential cause is unknown, though it 
is believed to be some germ as yet not isolated. Only a 
short exposure is necessary for its communication, and 
close proximity to the infected individual is not neces¬ 
sary. The disease is highly contagious from the onset 
of the catarrhal symptoms, and, as the patient is not 
ill and confined to the house at that time, measles is 
spread on all sides. After the disappearance of the 
rash and catarrhal symptoms, the communicability 
rapidly decreases, and during desquamation is but slight. 
Generally speaking, the duration of the infective period 
is three weeks. 

Children are usually attacked. Very young infants 
are not as susceptible to measles as those somewhat 
older, but in the very young the disease is a serious 
matter. The vast majority of those having measles are 
under 12 years of age. One attack usually produces an 

(227) 


228 


CLINICAL MEDICINE FQR NURSES. 


immunity to measles, but there are many exceptions to 
this rule, and two, and even three, attacks are not very 
uncommon. 

Symptoms (average attack). The disease is ushered 
in with symptoms of a diffuse catarrh of the upper 
respiratory tract. The patient has a “running” nose, 
“running” eyes, a sore throat, with redness of the ton¬ 
sils, and soft palate, a hoarse, harsh cough, and, in a 
day or so, some sputum. The catarrhal process spreads 
to the bronchial tubes, and bronchitis is present so fre¬ 
quently as to be looked upon as a symptom of measles, 
and not as a complication. 

The temperature rises gradually until the appearance 
of the rash, reaches about 104° as a maximum, and 
lasts in all usually about a week, varying from five to 
nine days. At first there is some dullness, pain in the 
back, headache, and general malaise, feelings that ac¬ 
company any moderate rise of temperature, and that 
present no characteristic features. Vomiting and diar¬ 
rhea are rarely seen save in the severer forms. 

Before the appearance of the rash there is but one 
sign that will point without question of doubt to measles. 
This sign is Koplik’s spots —bluish-gray spots seen 
against a red background on the mucus membrane of 
the cheeks and lips. 

The rash of measles appears, as a rule, on the fourth 
day of the disease. It is known as a maculo-papular 
rash. It appears first behind the ears, around the neck, 
and at the roots of the hair, as small, dark-red spots, not 
numerous, not elevated, and looking somewhat like flea- 
bites. In twenty-four hours the macules are numerous, 
and many have become papules. The rash spreads 
rapidly to the chest, arms, trunk, and eventually involves 


MEASLES. 


229 


the whole body within thirty-six hours. The papules, 
which have at first been single, may fuse, and, in so 
doing, often assume a crescentic form. At the height of 
the disease the patient may be so disfigured by the rash 
as to be unrecognizable. 

The skin is swollen, there is great itching, the eyes 
are red and very sensitive to light, and, as a rule, there 
is a conjunctivitis, with the formation of mucopus. Pain 
on swallowing, and swelling of the cervical glands are 
common. With the fading of the rash the temperature 
drops gradually, and reaches normal in from two to 
three days. 

Also, with the fading of the rash, desquamation or 
peeling sets in. This is first noticed on the face and 
neck and is in the form of fine, branny scales—never in 
large patches, as is the case in scarlet fever. As men¬ 
tioned before, desquamation lasts from one to two 
weeks—usually about ten days. 

Some cases of measles are so mild that were it not 
for other cases in the family or immediate neighbor¬ 
hood they could not be recognized. On the other hand, 
other cases are so severe that either the patient is over¬ 
come by the systemic poison within a few days, or else 
the whole force of the infection seems to be expended 
upon the lungs, and the case is more one of broncho¬ 
pneumonia than measles. Some severe cases have a 
hemorrhagic rash; others have convulsions and delirium, 
with all the signs of intense general poisoning. 

Complications. 

1. Bronchopneumonia. Frequent and dangerous. The 
symptoms that will cause the nurse to suspect a broncho¬ 
pneumonia are: 


230 


CLINICAL MEDICINE FOR NURSES. 


(a) Rise in temperature. 

( b ) Rise in pulse-rate. 

(c) Rise in rate of respiration. 

( d ) Increase in cough, and, in older children, in 

expectoration. 

( e ) Appearance of slight cyanosis in young chil¬ 

dren or in the very delicate. 

2. Otitis media. Also frequent, but not as dangerous 
as bronchopneumonia. 

Older children will usually complain of pain in the 
ear, and thus the nature of the trouble can be suspected, 
but in very young children and in infants the nurse must 
be constantly on guard for some change in her patient 
that will make her suspect otitis media. 

In the very young the following symptoms are 
suggestive: 

(a) Rise in temperature not traceable to the bowels 

or lungs. 

( b ) Fretful and persistent crying. 

( c ) Difficulty in taking the bottle (in infants). 

(d ) At times evident pain and tenderntss in the 

region of the ear. 

With such symptoms the nurse should at once call the 
physician, who will make the diagnosis by examination 
of the ear through an ear-speculum. 

Diphtheria and scarlet fever may complicate measles. 
Kidney complications (nephritis) are rare, as are heart 
affections. Laryngitis is present in practically every 
case. When membranous laryngitis occurs it is caused 
either by the diphtheria bacillus or the streptococcus, 
and the symptoms are those described under “Laryngeal 
Diphtheria.” 


MEASLES. 


231 


Prognosis. The outlook in the better class of private 
practice is generally good in children over 3 years of 
age. In those younger, mortality is fairly high. In 
those over 3, the average mortality is from 4 to 6 per 
cent., and often it does not reach these figures. 

In institutions the picture is reversed, largely because 
the patients come from the poorer walks of life, are 
underfed, and have poor resistance. Here measles plays 
great havoc, in some institutional epidemics the mortal¬ 
ity ranging from 15 to 35 per cent. 

Prophylaxis. Room quarantine is required by law 
for a variable period depending upon the ruling of the 
local board of health. As the details for maintaining 
this quarantine are the same (save in point of time) as 
for scarlet fever and diphtheria, they have been given 
but once, and will be found in the chapter on Scarlet 
Fever. 

Treatment. Measles is a self-limited disease, and 
we have no means at our command to shorten or modify 
it. Treatment is, therefore, wholly symptomatic. 

The room should be darkened (especially in summer) 
by means of blinds or green shades, and the electric bulb 
or lamp covered with a red shade, in order to lessen all 
possible irritation of the eyes. An initial purge with 
calomel followed by a saline or castor oil is usually given. 
If the eyes are painful, ice-cold cloths frequently give 
relief, and the mucopus appearing as a result of the 
conjunctivitis should be wiped away with small bits of 
old linen moistened in a solution of boric acid. Vase¬ 
line may be freely applied to the lids. Vaseline or cocoa 
butter should be rubbed over the child’s entire body in 
order to allay itching. 


232 


CLINICAL MEDICINE FOR NURSES. 


The diet should at first be liquid. Later in the dis¬ 
ease eggs, toast, cereals, gruels, ice cream and crackers 
may be added. After the appearance of the rash a daily 
warm bath should be given in addition to the inunction 
above referred to. 

The cough will usually need some treatment. Gen¬ 
erally, opium in some form is given, either as codeine or 
heroin, combined with an expectorant mixture. 

In cases of excessively high fever (105° or over) re¬ 
course is usually had to cold sponges, with alcohol 1 
part, water 3 parts. With failing heart, stimulation is 
indicated, though there is rarely need for this save in 
the presence of bronchopneumonia, when the treatment 
becomes that of the complication rather than that of 
measles. The eyes must not be subjected to any undue 
strain for several weeks after measles, and during and 
after convalescence the child must be carefully watched, 
and every precaution taken against “catching cold,” for 
the mucous membrane of the entire respiratory tract is 
in a condition of lowered resistance, and is particularly 
susceptible to all manner of infection. 

If cough continues for any considerable length of 
time after recovery from measles, the possibility of 
tuberculosis must be borne in mind, this disease being 
one of the most frequent sequels of measles. 


CHAPTER XXV. 

DIPHTHERIA. 

Diphtheria is “an acute infectious contagious dis¬ 
ease characterized by the formation of a gray-white 
membrane on the tonsils, uvula, and soft palate, and by 
constitutional symptoms of varying intensity.” 

Etiology. The Klebs-Loeffler bacillus, discovered 
in 1883. Diphtheria is very contagious. Short ex¬ 
posure is all that is necessary for infection to take place, 
and in addition the disease is spread by “carriers”— i.e., 
persons having virulent diphtheria bacilli in their 
throats, but because of a natural or acquired immunity, 
not ill with the disease. 

Symptoms. The incubation period of diphtheria is 
from twelve hours to three days. While diphtheria may 
occur on any mucous membrane where the bacilli lodge 
and develop (nose, vagina, stomach, etc.), it is very rare 
to see the disease anywhere save in the pharynx or 
larynx, and these two forms only will be considered 
here. 

1. Pharyngeal Diphtheria. The onset is reasonably 
sudden, with chilliness, headache, fever, not particularly 
marked. It is uncommon to see a temperature over 102°. 

Within twenty-four hours the throat becomes sore. 
At first it is red, but soon spots of gray or dirty white 
appear on one or both tonsils. These increase in num¬ 
ber, unite, and spread to the uvula and soft palate. In 
a fully developed case the back of the mouth is often 
seen to present an arch of grey membrane, reaching 

(233) 


234 


CLINICAL MEDICINE FOR NURSES. 


from tonsil to tonsil. The membrane is thick and 
tenacious, and when pulled off leaves a raw, bleeding 
surface. As the disease progresses, prostration becomes 
more marked, and signs of heart weakness are frequent. 
The membrane may disappear as a result of treatment, 
or, in unfavorable cases, may spread to the nose or 
larynx. Cultures taken from the throat show the pres¬ 
ence of diphtheria bacilli in large numbers. The course 
of diphtheria is variable, lasting from six days to three 
weeks, but has been wholly changed since the introduc¬ 
tion of treatment by antitoxin. 

2. Laryngeal Diphtheria. The general symptoms are 
the same as those of pharyngeal diphtheria, save that, 
as a rule, prostration is more pronounced. 

The first local symptom is a hoarse, brassy cough. 
The voice may be merely husky, or the patient may not 
be able to speak above a whisper. If the membrane con¬ 
tinues to spread over the larynx, dyspnea sets in, due to 
obstruction to the free passage of air. Cyanosis sets in, 
slight at first, but, in severe cases, gradually increasing 
until the entire face looks dusky, the patient gasps for 
every breath, the pulse is rapid, small and weak, and the 
entire body covered with a cold sweat. In untreated or 
very virulent cases the larynx may be entirely filled by 
the membrane, and death from suffocation result. 

Complications. 

1. Nephritis. Almost a constant occurrence, and due 
to the action on the kidney of the toxin of the diphtheria 
bacillus. Usually transitory; not serious; and diagnosed 
by the urinary findings. 

2. Cervical adenitis. The glands of the neck are very 
frequently involved. They are often swollen and tender. 
Occasionally they break down and suppurate. 


DIPHTHERIA. 


235 


3. Bronchopneumonia. This complication is always 
serious. The gravity depends upon the age of the pa¬ 
tient (if a child, the younger it is the more serious is 
the complication) and the severity of the diphtheritic 
attack. Bronchopneumonia is particularly apt to com¬ 
plicate cases of laryngeal diphtheria. For symptoms of 
this condition, see chapter on Bronchopneumonia. 

4. Various paralyses. Very important. Due to a 
definite toxic action of the diphtheria poison upon the 
nervous system. Many varieties of paralysis may occur, 
chief among them being: 

(а) Palatal paralysis (soft palate), causing a nasal 

voice. 

(б) Paralysis of any of the eye-muscles. 

(c) Paralysis of any of the accessory muscles of 
respiration; if at all extensive, this is char¬ 
acterized by a peculiar sighing respiration. 

5. Heart-failure. Most important of all. The toxin 
of the diphtheria bacillus has a very definite selective 
action upon the heart-muscle, causing a degeneration of 

. the muscle fibres—a toxic myocarditis. Myocarditis is 
suspected from the rate and quality of the pulse, and 
from the fact that any physical exertion has a marked 
effect upon the circulation. Neither extreme of pulse- 
rate is of good omen, for “a rapid pulse-rate is always 
cause for alarm, and a slow pulse-rate an indication of 
serious trouble.” 

6. Vomiting. When this occurs early in the disease 
it may be due to the temperature and malaise that accom¬ 
pany any acute infectious disease. When vomiting 
occurs late in the disease, it is a very important and very 
dangerous symptom, as it points to beginning degenera¬ 
tion of the vagus nerve. 


236 


CLINICAL MEDICINE FOR NURSES. 


Prognosis. The outlook in diphtheria is always 
grave, though its course and termination have been so 
entirely revolutionized by treatment with antitoxin that 
this factor must always be held in the foreground. The 
gravity of prognosis and the rate of mortality are in 
direct proportion to the delay in administering antitoxin. 

Kossel has shown that when antitoxin is injected 
on the first sign of the disease the percentage of re¬ 
coveries is 100. In this every hour counts. 

Out of 2428 cases reported by Hilbert, the percentage 
of deaths varied with the day on which antitoxin was 
administered, as follows: 


Day of administration Mortality 


First day . 

. 2.2 

per cent 

Second “ . 

. 7.6 

a a 

Third “ . 

. 17.1 

it u 

Fourth “ . 

. 23.8 

u a 

Fifth “ .. 

. 33.9 

tt a 

Sixth ~ . 

. 34.1 

a tt 

After sixth day. 

. 38.2 

a a 


(Vaughan.) 

The prognosis is always much graver in laryngeal 
than in pharyngeal cases. 

Treatment. The treatment of diphtheria can be 
divided into two classes: 

(1) General treatment. 

(2) Specific treatment— i.e., antitoxin. 

1. General Treatment. ( a ) Prophylactic . The pa¬ 
tient is to be isolated, as described in the chapter on 
Scarlet Fever, and quarantine is to be maintained until 
release is permitted by the board of health, the period 
varying in different communities, but being in all cases 
dependent upon cultures from the throat of patient and 
nurse showing no diphtheria bacilli. 










DIPHTHERIA. 


237 


( b ) General Management. Bed is to be insisted upon 
in all cases, and rest in the recumbent position is very 
important, owing to the toxic action of the diphtheritic 
poison on the heart. The nurse must be careful not to 
let the patient sit up suddenly (as children are apt to 
do), as cases are on record where such exertion has 
caused sudden giving out of the heart, with immediate 
death. The bowels are to be kept open, and the mouth 
clean with some mild antiseptic wash. Gargling is not 
advisable, as it practically always necessitates sitting up. 

Food should be liquid and semi-solid, bland, easily 
digestible, and given frequently in small amounts. 
Swallowing is at first usually very painful, and it may 
be very difficult to get patients, especially children, to eat 
a sufficient amount. In toxic cases, stimulation is to be 
resorted to, differing in no wise from that given in any 
disease complicated by heart-failure. 

For the paralyses following diphtheria, strychnia 
seems to exert a more beneficial effect than any other 
drug. The patient should be kept in bed until convales¬ 
cence is fully established, because of the danger of sud¬ 
den heart-failure even after all signs of active diph¬ 
theritic disease have disappeared. Cold to the throat in 
the form of cold cloths is often beneficial. The ice-bag 
is often very efficient in relieving pain. Opiates may 
have to be given. 

2. Specific Treatment. There is probably no more 
brilliant achievement in internal medicine than the 
triumph gained over diphtheria by the discovery of diph¬ 
theria antitoxin by von Behring in 1890. 

Antitoxin. Antitoxin is obtained by injecting horses 
with gradually increasing doses of diphtheria toxin, 


238 


CLINICAL MEDICINE FOR NURSES. 


until an immunity has been established, so that the 
animal can withstand, with no harmful effects whatso¬ 
ever, doses that would have proved immediately fatal if 
given at first. When the horse is sufficiently immunized 
he is bled, and in the blood-serum is found the diphtheria 
antitoxin— i.e., a substance which is capable of neutral¬ 
izing and rendering harmless the diphtheritic poison cir¬ 
culating in the patient’s blood. The measure adopted 
for estimating the amount of antitoxin is the “unit.” 
The serum of the horse is standardized, and put up in 
syringes ready for use, each holding a certain number of 
units of antitoxin—500, 1000, 2000, 5000, 10,000, as the 
case may be. Diphtheria being strictly a toxic disease 
{i.e., the poison manufactured by the diphtheria bacilli 
being the one harmful factor), if enough antitoxin 
is injected to neutralize all the toxin circulating in 
the blood, the patient has an excellent chance for 
recovery. 

(a) Prophylactic Treatment with Antitoxin. It is 
customary to give the nurse and all members of the 
family a preventive injection of antitoxin—from 500 to 
1000 units, according to the age of the individual to 
whom it is given. This prophylactic injection estab¬ 
lishes an immunity to diphtheria which lasts about three 
weeks. 

(b) Active Treatment with Antitoxin. Antitoxin 
should be administered as soon as the diagnosis is made, 
and, in doubtful cases, in the absence of a positive diag¬ 
nosis, because if the case is one of diphtheria it will do 
good, while if the case is one of follicular tonsillitis, no 
harm will result, and because mortality from diphtheria 
increases in direct proportion to delay in the adminis¬ 
tration of antitoxin. 


DIPHTHERIA. 


239 


Antitoxin is administered hypodermically, the loose tis¬ 
sue of the back below the angle of the scapula being the 
favorite site of injection. The dose depends upon the 
judgment of the physician. Some believe in relatively 
small doses (2000 to 5000 units), others in moderately 
large doses (10,000 to 30,000 units), and still others in 
enormous doses (50,000 to 100,000 units). From this it 
will be apparent that, practically speaking, there is no such 
thing as an overdose of antitoxin. If the symptoms do 
not improve after the first injection, another is given from 
eight to twelve hours later, and subsequent doses are given 
as indicated. Where antitoxin has a beneficial effect, in 
from six to eighteen hours the membrane is seen to grow 
less, and finally to disappear; the temperature drops, and 
all signs of toxemia are reduced in intensity, the throat be¬ 
ing often almost normal within three or four days. In 
more severe cases, a longer time is necessary for recovery; 
and in the fulminant cases, or in those in which antitoxin 
administration has been delayed until the entire body is 
flooded with poison, death ensues. It must be clearly 
understood that antitoxin can only exert its antitoxic ef¬ 
fect upon the toxin that is circulating in the blood stream. 
Antitoxin has no effect upon toxin that has already at¬ 
tached itself to the body cells. Hence, when administra¬ 
tion of antitoxin is delayed, while it may neutralize all 
free toxin found, too much poison may have already at¬ 
tached itself to the body cells to enable the patient to over¬ 
come its action. 

In cases of laryngeal diphtheria, in addition to anti¬ 
toxin administration (always in larger dosage than in 
pharyngeal cases), mechanical means may be necessary 
to relieve the blocking up of the larynx, and consequent 


240 


CLINICAL MEDICINE FOR NURSES. 


death of the patient from suffocation. These are two in 
number: 

1. Intubation. By means of a special instrument for 
its insertion, devised by the late Dr. Joseph O’Dwyer, of 
New York, a hollow tube is passed into the larynx until 
it is between the vocal cords, where it lodges, and is held 
in place by means of a groove at its upper end. The 
patient is able to breathe through the tube until the mem¬ 
brane lessens in amount and the larynx is again clear, 
when the tube is extracted if the patient fails to cough 
it out. 

2. Tracheotomy. If intubation is impracticable, an 
opening is made in the trachea, and a tracheotomy tube 
inserted, through which the patient can get air. 


CHAPTER XXVI. 


ANTERIOR POLIOMYELITIS (INFANTILE 
PARALYSIS). 

Definition. An acute infectious disease occurring 
both in epidemics and sporadically, due to a filtrable 
and cultivable virus, involving different parts of the 
nervous system, often localizing especially in the ante¬ 
rior horns of the gray matter of the spinal cord (polio¬ 
myelitis anterior), but also localizing in the cerebrum, 
in the medulla oblongata, in the cerebellum, and in the 
meninges, to a variable extent in different cases. Since 
the epidemic of poliomyelitis in New York in 1916, the 
medical thought of the country has been markedly con¬ 
centrated upon this disease. 

Etiology. After many experiments it has been estab¬ 
lished that the juices of the nervous system of an in¬ 
fected animal when filtered through porcelain or some 
other filter, are still able to infect monkeys. Hence the 
disease is due to a filtrable virus. This virus is most 
concentrated in the nervous system of the patient, but is 
also to be found in the mesenteric glands, and in the 
tonsils and throat. “The virus stands cold well, retain¬ 
ing its virulence when kept frozen for at least 11 days. 
It is enfeebled by a temperature of 45° C., and is killed 
after heating for half an hour at 55° C. It is not killed 
by drying. It can live for some time in sterile water or 
sterile milk, apparently without multiplication” (Bar¬ 
ker). The transmission of the infection by the stable- 
fly, insects, fomites, etc., is still a debatable point. The 

16 (241) 


242 


CLINICAL MEDICINE FOR NURSES. 


disease is present chiefly in mid-summer and in the fall, 
though cases occur at all seasons of the year. The vast 
majority of those attacked are children from 1 to 4 years 
of age. 

Pathology. Formerly it was believed that destruc¬ 
tion of the anterior horn cells of the spinal cord was the 
sole characteristic lesion of poliomyelitis. Latterly it 
has been found, however, that the lesions of a localized 
or generalized meningitis may be present, the process 
being situated in the cerebrum, cerebellum, or medulla 
oblongata, as the case may be. In many cases (the 
majority of those positively recognized), the anterior 
horn cells are the structures most damaged. They show 
signs of degeneration, and as a result the motor nerve 
fibres arising from these cells degenerate, with result¬ 
ant paralysis of the muscles supplied. Some of the 
motor cells in the anterior horns of the cord are wholly 
destroyed; others recover partially; still others recover 
completely. This accounts for the gradual recovery 
from the paralysis; for as function is regained on the 
part of the motor cells, regeneration of the nerve fibres 
takes place, and impulses that cause the muscle to con¬ 
tract are again transmitted. 

Symptoms. The incubation period is usually about a 
week. In the typical case, the child is taken suddenly ill 
with symptoms in no wise characteristic. They are often 
thought to be due to tonsillitis or influenza. There is 
usually vomiting, sometimes diarrhea, moderate fever 
ranging from 101° to 103°, with the usual symptoms 
that accompany a febrile disturbance. There may be 
pain in the limbs, rigidity of the neck, and symptoms 
suggestive of meningitis ( q.v .). The characteristic fea¬ 
ture of the typical case is paralysis, which appears within 


ANTERIOR POLIOMYELITIS. 243 

a week of the onset. In infants and very young children 
this paralysis may not be noticed for several days, 
though obviously present when sought. In older chil¬ 
dren, paralysis is, of course, noticed as soon as it ap¬ 
pears. At first the paralysis may seem to affect one or 
more limbs in their entirety, but it soon manifests its 
rather characteristic distribution. The muscles are usu¬ 
ally affected in groups (corresponding to the particular 
segment of the spinal cord in which the anterior horn 
cells have been most damaged), and are rarely affected 
singly. Thus, the peroneal muscles on the outer side of 
the leg may be involved, the extensor muscles of the 
front of the thigh, the deltoid group covering the shoul¬ 
der, some of the muscles of the forearm, etc. Usually 
more than one group is involved at first. The paralysis 
is what is termed “flaccid,” i.e., the paralyzed limb lying 
quite loosely. There is no disturbance of sensation, 
though at times the limb may be cool to the touch and 
slightly edematous. 

The actual febrile period lasts usually from a few 
days to two weeks. In bad cases the patient may be 
overwhelmed with toxemia, and die in a few days, or 
else death may ensue as a result of paralysis of the 
muscles of respiration. 

After the acute febrile period has passed, the stage of 
repair begins, which may last as long as two years. It 
is important to remember that paralysis is always most 
extensive at first, that practically . every case shows 
marked improvement over the condition as it existed at 
first, and that complete recovery occurs in about 20 per 
cent, of the cases. 

In the course of epidemics many atypical cases are 
seen, some showing damage to the various cranial 


244 


CLINICAL MEDICINE FOR NURSES. 


nerves, as shown by facial and ocular paralyses of vary¬ 
ing degrees of severity, others giving symptoms of a 
multiple neuritis (pain along the course of certain 
nerves, sensitiveness to touch and paralysis), still others 
showing symptoms almost characteristic of meningitis 
(q.v.). In the course of epidemics stress must be laid 
upon the abortive forms of poliomyelitis, where no 
paralysis occurs, although the general symptoms of ill¬ 
ness may be present, i.e., fever, together with symptoms 
suggesting a respiratory, meningeal, or general influenzal 
infection. Every transition stage is noticed between 
these non-paralytic forms and those showing most ex¬ 
tensive loss of function. It is now believed that in large 
epidemics of poliomyelitis from one-third to one-half of 
all the infections are abortive forms. 

Prognosis, The death-rate varies between 10 and 40 
per cent., according to statistics of various epidemics. 
Death usually occurs on the fourth or fifth day, and the 
mortality is greater in adults than in children. 

Prophylaxis, At present, prophylaxis does not seem 
to be of much service. The modes of transmission of 
the virus of the disease are insufficiently known, and in 
epidemics the great number of undiagnosed and abor¬ 
tive cases as well as the numbers of healthy adults act¬ 
ing as carriers make any attempt at satisfactory isola¬ 
tion and quarantine practically impossible. The patient 
should, of course, be isolated, and other children in the 
family kept away from school for at least eight weeks. 
All discharges from the nose, throat, bladder, and rec¬ 
tum should, when possible, be destroyed by burning. 
Those individuals not affected should have the nose and 
mouth sprayed with some mildly antiseptic solution. In 
times of epidemics schools should be closed, children’s 


ANTERIOR POLIOMYELITIS. 


245 


parties not held, and all children should be watched care¬ 
fully to see that they never use any article belonging to 
any other child. Disinfection of the sick-room is im¬ 
perative, and, if possible, fumigation of the entire 
premises after a case of poliomyelitis is desirable. 

Treatment. During the acute stage of the disease the 
management is that of any febrile affection. Bed, liquid 
diet, attention to the bowels and kidneys, cold or heat 
applied to painful areas, and sedatives when indicated. 
The management of the stage of repair in poliomyelitis 
is a very complicated matter, and cannot be taken up in 
detail. Much depends upon the competence of the 
nurse, and upon the zeal with which she executes the 
physician’s orders as to the different measures to be 
carried out. These orders should be given in great de¬ 
tail, preferably in writing, as should they be misunder¬ 
stood and wrongly carried out, irremediable harm may 
result. 

The general management of the^ stage of repair in 
poliomyelitis, consists in the prolonged and judicious 
application of the following therapeutic agencies: 

1. Electricity. 

2. Massage. 

3. Local heat. 

4. Exercise. 

5. Orthopaedic apparatus (braces). 

6. Surgical operations planned to help the damaged 

muscles in the resumption of their proper 
function. 


CHAPTER XXVII. 


EPIDEMIC CEREBROSPINAL MENINGITIS. 

This disease occurs both in epidemics and in single 
scattered cases. It is most prevalent in the winter and 
spring months, occurs most frequently in crowded quar¬ 
ters where there is faulty hygiene, and may be com¬ 
municated by the secretions of the nose, mouth, and 
conjunctiva. Whether it can be communicated by in¬ 
sects has as yet not been determined. 

Etiology. The disease is caused by a specific germ 
—the diplococcus intracellularis meningitidis of Weich- 
selbanm. 

This organism is always present in the bodies of the 
leukocytes in the spinal fluid in epidemic meningitis, and 
has also been found in the secretions of the nose, mouth, 
and eye. 

Pathology. The characteristic changes found are 
limited to the meninges of the brain and spinal cord. 

1. Brain. The meninges (membranes) are congested 
and inflamed. There is an exudate of serum and pus 
at the edges of the brain, and extending over the upper 
and outer surface (the “convexity” of the brain). The 
brain-tissue itself is the seat of congestion, hemorrhages, 
thrombi, and small abscesses. 

2. Cord. The meninges and body of the cord are 
affected in a manner similar to those of the brain. The 
central canal of the cord and the ventricles of the brain 
are dilated, the amount of spinal fluid is increased, the 

(246) 


EPIDEMIC CEREBROSPINAL MENINGITIS. 247 


fluid itself is turbid, and is under much greater pressure 
than normal. 

Symptoms. These vary greatly in various epidemics. 
In a typical attack, the onset is sudden, with severe 
headache, vomiting, and temperature from 102° to 104°. 
The headache increases in intensity, and becomes agoniz¬ 
ing. There is sensitiveness to light, and sometimes to 
sound, the neck becomes stiff, and the head is retracted. 
Any attempt to bend the head forward causes excruciat¬ 
ing pain. The reflexes (knee-jerk, wrist-jerk, etc.) are 
markedly increased. Kernig’s sign is present (inability 
to extend the leg fully when the thigh is placed at right 
angles to the trunk). 

The pupils are at first contracted, and usually equal. 
There may be an eruption of herpes on the lips, or else 
herpes zoster (shingles) may appear on the body. All 
the signs hitherto enumerated are those of cerebral irri¬ 
tation. With the further progress of the disease, the 
signs of cerebral depression set in. In a fully 
developed case the patient is in a semi-conscious, 
delirious, stuporous, or comatose condition, usually lying 
on the side in a crouching position, the head retracted, 
the legs drawn up, the arms bent at the elbows— i.e., 
nature seeking the position of greatest relaxation. The 
high fever may fall to subnormal; the patient may be 
quiet, or else toss restlessly about. When aroused, 
he may show signs of irritability and excessive sen¬ 
sitiveness. There is usually an increase in the 
leukocytes. 

The course of the disease is very varied. Excessively 
severe cases may result in death within a few hours; 
other cases may last many weeks, the fever running an 
irregular course. Usually the disease is at its height 


248 


CLINICAL MEDICINE FOR NURSES. 


for five or six days, after which the symptoms grad¬ 
ually abate. 

The complications of cerebrospinal meningitis are not 
numerous, but are very serious. 

1. Otitis. Common, and often resulting in deafness, 
which is absolute and incurable. If the patient is very 
young, deaf-mutism is the result. 

2. Pneumonia. Frequent, and very fatal. 

3. Hydrocephalus. Not so frequent, but very fatal. 

Prognosis. The outlook is always very grave. Pre¬ 
vious to the discovery of antimeningitis serum the mor¬ 
tality was excessively high—80 per cent, or more. Since 
this serum has been used, mortality has been greatly re¬ 
duced, but still remains about 25 per cent. 

Lumbar Puncture. Lumbar puncture is used as a 
method of diagnosis and as a method of treatment. It 
is a procedure that the nurse will never be called upon 
to carry out, but it is one that she will witness, and in 
the performance of which she will lend assistance. 
Therefore, she should understand what is being at¬ 
tempted, and what information is being sought from the 
procedure. 

By lumbar puncture is meant the insertion of a hollow 
needle into the spinal canal, and the withdrawal through 
the needle of the spinal fluid for the purposes of: 

(1) Examination. 

(2) Lessening intracranial pressure. 

(3) Both of the preceding. 

(4) As a preliminary measure to the injection of 

certain drugs or sera. 

For the performance of lumbar puncture the nurse 
in attendance should have the following articles in 
readiness. 


EPIDEMIC CEREBROSPINAL MENINGITIS. 249 

(1) Needles—sterilized. 

(2) Iodine. 

(3) Sterile gauze and sponges. 

(4) Gloves for the physician. 

(5) Novocain, 0.5 per cent, solution, 5 c.c. 

(6) Sterile test-tubes (2) to receive fluid. 

(7) Collodion. 

The patient is turned on the side, with his back to¬ 
ward the operator, and drawn as near as possible to 
the edge of the bed. The thighs are flexed on the 
trunk, and the legs on the thighs, and the back is 
“bowed’’ forward as much as possible, so as to in¬ 
crease the space between the vertebrae. The nurse 
usually holds the patient in this position while lum¬ 
bar puncture is being performed, and the procedure 
is, as a rule, simple and rapid for one accustomed 
to it. 

The site chosen for lumbar puncture is between 
the second and third, or third and fourth, lumbar 
vertebrae. 

Normal spinal fluid is absolutely clear, and escapes 
from the needle at the rate of about 8 drops to the 
minute. If the fluid is under pressure, it may run in 
a steady stream, or spurt several feet. 

The following statements are true in a general way: 

If fluid is clear and under no excessive pressure, normal; if 
fluid is clear and under excessive pressure, tuberculous menin¬ 
gitis; if fluid is turbid and under excessive pressure, probably 
epidemic cerebrospinal meningitis or some septic meningitis; if 
fluid is blood-stained, no immediate inference can be drawn. 

Treatment. Prophylaxis. Should be the same as 
for typhoid fever ( q.v .). 


250 


CLINICAL MEDICINE FOR NURSES. 


Thanks chiefly to the work of Dr. Simon Flexner, of 
the Rockefeller Institute in New York, a serum has been 
manufactured that greatly detracts from the terrors of 
epidemic cerebrospinal meningitis. This is antimeningitis 
serum. 

Antimeningitis serum is obtained, as is diphtheria anti¬ 
toxin, from horses which have gradually been immunized 
to large doses of the poison of the germ causing cerebro¬ 
spinal meningitis. The scram is of value in this disease 
alone, and is of no use in any other form of meningitis. 

A lumbar puncture is done, and if the diplococci of 
cerebrospinal meningitis are found in the spinal fluid, the 
serum is injected intraspinally. More than 30 c.c. of the 
serum are never given at one dose. Injections are given 
daily for four days, and the signal for cessation of treat¬ 
ment is failure to find any more diplococci in the cells 
of the spinal fluid. Subcutaneous injections of serum 
are worthless but intraspinal injections are often supple¬ 
mented by intravenous injections with good results. 

General Treatment. The remainder of the treat¬ 
ment of this disease is purely symptomatic, and consists 
in giving the patient as much nutritious food as possible, 
in keeping the bowels well open, in giving sedatives for 
pain, and in giving stimulants when needed. 


CHAPTER XXVIII. 

SYPHILIS* 

Syphilis is a specific infectious disease caused by the 
presence in the tissues of the infected individual of the 
Spirocfazta pallida. 

A nurse is practically never called upon to care for a 
case of syphilis as such, for those cases do not require 
nursing. She will, however, be called upon to nurse 
many individuals who have or have had syphilis, and 
she should realize and appreciate the enormously impor¬ 
tant role played by this disease in predisposing to or 
actually bringing about other pathological conditions. 
A very brief review of syphilis itself will be given, and 
then a few words will be said concerning its causal rela¬ 
tionship to other diseases. 

It has been determined beyond a doubt that syphilis 
was first brought to Europe from Espanola or Haiti in 
1493 by the sailors with Columbus on his first voyage of 
discovery. The disease began to be noticed during the 
invasion of Italy by Charles VIII. of France in 1494, in 
order to conquer Naples, with an army of mercenaries 
from all parts of Western Europe. With the defeat of 
Charles’s army the disease was traced by the scattering of 
his troops, and appeared in France, Germany, and 
Switzerland in 1495, in Holland and Greece in 1496, in 
England and Scotland in 1497, and in Hungary and Rus¬ 
sia in 1499. 

As is usual with the initial appearance of a disease 
among a people unused to its presence, during the first 

* For the subject matter of this chapter I am mainly indebted 
to the very interesting monograph, “Syphilis as a Modern Prob¬ 
lem,” by Dr. W. A. Pusey, of Chicago. (251) 



252 


CLINICAL MEDICINE FOR NURSES. 


decades of its prevalence syphilis raged with extraordi¬ 
nary severity; but at the end of fifty years Europeans 
had developed a certain amount of immunity to it; and 
the cases becoming milder and more chronic, assumed the 
type seen today. 

Syphilis is usually acquired during sexual intercourse, 
and the first sign of it, the “initial lesion” or chancre, is 
therefore most frequently to be found on the genitals. 
Infection cannot take place unless the mucous membrane 
is broken, but the abrasion may be of microscopic size. 
Individuals in the so-called “secondary” stage of the 
disease, with “mucous patches” in their mouths, can 
infect others by kissing, the initial lesion then showing 
itself on the lips or in the mouth. Shamberg reports a 
case where a young man with a chancre of the lip in¬ 
fected 7 young girls at a party where kissing games were 
played. 

The course of syphilis falls naturally into several 
stages. A brief summary of these stages may serve to 
give a clear picture of the disease. 

1. Incubation Period. From the time of infection to 
the appearance of the initial lesion. Approximately four 
weeks. 

2. Primary Stage. Lasting about six weeks. During 
this period the chancre, which is a small ulcer, with a 
hard base, and covered by a small amount of clear secre¬ 
tion, develops and disappears; the infection gradually 
invades the entire body, and the period is abruptly 
brought to an end by the appearance of the eruption or 
rash. 

3. Secondary Stage. Begins with the appearance 
of the rash, and ends only with the disappearance of 
evidences of an active systemic infection. It may last 


SYPHILIS. 


253 


for a few weeks, several months, or more than a year, 
and may be accompanied by slight fever, some loss of 
weight, and a mild degree of general malaise. The rash 
may assume one of many forms. 

4. Tertiary Stage. Characterized by the presence of 
lesions due to isolated local syphilitic processes, situated 
anywhere in the body, and affecting most frequently the 
blood-vessels, liver, brain, central nervous system, and 
bones. 

Syphilis thus presents resemblances to three types of 
disease. First, a local infection characterized by a local 
lesion, the chancre; second, it resembles the acute 
specific infections, especially the eruptive fevers; third, 
by the formation of localized foci of inflammation, it 
resembles tuberculosis. The secondary manifestations of 
syphilis are those of an acute systemic disease. The ter¬ 
tiary manifestations are those of a chronic disease 
sharply localized in its activity. 

Syphilis rarely directly kills the patient. Its most 
dreaded effects are remote, and are exerted upon various 
organs and tissues of the body. 

A few historical facts of very recent date may be of 
interest as showing the epoch-making contributions of 
the twentieth century to the knowledge of this impor¬ 
tant disease. 

In 1903 Metchnikoff and Roux demonstrated that apes 
could be inoculated with syphilis. 

In 1905 Schaudinn and Hoffman discovered the spiro- 
chseta pallida, which is the sole cause of syphilis. 

In 1906-7 Wassermann, Neisser, and Bruck developed 
the “Wassermann reaction” as a test for the presence and 
diagnosis of syphilis, which has enabled many thousands 
of cases to be recognized and treated that could not have 


254 


CLINICAL MEDICINE FOR NURSES. 


been diagnosed by any of the previous methods at the 
physician’s command. 

In 1909-10 Ehrlich discovered and gave to the profes¬ 
sion “606,” or “salvarsan,” now largely supplanted by the 
substance known as arsphenamin, a preparation of arsenic 
for the treatment of syphilis. 

Hereditary Syphilis. Syphilis can be, and often is, 
directly transmitted from the mother to the child she is 
bearing. If the child is born actively syphilitic, it usually 
dies in a few weeks at most, and during its life it is 
acutely ill. The skin and mucous membranes are 
markedly affected by the syphilitic eruption; there is 
severe running at the nose, and laryngitis; the nasal dis¬ 
charge is purulent, and the child snuffles and breathes 
with difficulty. Because of the laryngitis it frequently has 
a characteristic high-pitched harsh cry. It is emaciated, 
and the liver and spleen are usually enlarged. 

If the child is born infected, but with no active symp¬ 
toms, these begin in from two to six weeks. Snuffles is 
usually the first symptom, to be followed by those de¬ 
scribed in the preceding paragraph. If treated, many of 
these cases recover. 

For a woman, to bear a syphilitic child, she must be her¬ 
self actively syphilitic. If the disease is inactive a syph¬ 
ilitic mother will bear healthy children, while later, if the 
disease reawakens, she will bear syphilitic children. 

Prophylaxis of Syphilis. This cannot be dealt with 
here. The question is a vast one, indeed, and is as much 
sociological as medical. Syphilis and its spread are so 
intimately connected with the questions of prostitution, 
loose morals, the relations of the sexes, that to touch the 
question at all would be to plunge into very deep water. 


SYPHILIS. 


255 


Treatment of Syphilis. For several centuries mer¬ 
cury has been known as a specific remedy for the syphi¬ 
litic poison. It has been administered by inunction, by 
mouth, and hypodermically. It is still one of the main¬ 
stays of treatment. 

Arsphenamin is the newest substance for combating 
syphilis. Ehrlich hoped that by the administration of ars¬ 
phenamin intravenously he could definitely cure syphilis. 
This hope has not been fully realized. Valuable as ars¬ 
phenamin is, it has been found that the best results are 
obtained when it is combined with vigorous treatment 
with mercury. 

Syphilis in Its Relationship to Other Diseases. 

This aspect of syphilis is one of the most important to 
be considered. Diseases directly or remotely due to the 
syphilitic poison may appear many years after all symp¬ 
toms and signs of syphilis have disappeared, and, up to 
the present time, no method of treatment has been de¬ 
vised that will prevent the later effects of this disease. 

By the action of the syphilitic poison on the blood¬ 
vessels, arteriosclerosis is frequent, and there are authori¬ 
ties who assert that every case of aneurysm not due to 
injury, has, as at least one of its causative factors, syph¬ 
ilis. As a result of arteriosclerosis the kidneys are dam¬ 
aged, and the heart overtaxed, giving rise to the condi- 
’ tion described as cardiovascular-renal disease. 

It has been shown beyond a doubt that locomotor 
ataxia and paresis (softening of the brain) are always 
late results of syphilis. These two diseases, both very 
serious and incapable of cure (arrest being the best re¬ 
sult attainable by any form of treatment), form one of 
the saddest chapters occurring in middle life as a remote 


256 


CLINICAL MEDICINE FOR NURSES. 


effect of a syphilitic infection received perhaps a quarter 
of a century before. 

By its action in lowering bodily resistance, syphilis plays 
a part in the causation of almost every disease known to 
man. 

Sir William Osier has said that “the man that knows 
syphilis in all its manifestations, knows most of medi¬ 
cine” ; and it is important for the nurse to appreciate the 
role played in the human body by this disease. One of 
the reasons that syphilis has so many remote effects is that 
the disease in its active form is singularly yielding to treat¬ 
ment. Symptoms disappear rapidly, and apparent health 
returns. The patient realizes with difficulty that from one 
to three years of treatment are necessary to thoroughly 
eradicate the spirochseta pallida. With a return of physi¬ 
cal well-being treatment is maintained half-heartedly, if 
indeed it is not wholly abandoned, and many of the spiro- 
chseta, unharmed, bury themselves deep in the tissues, 
where they hibernate in safety, to make their activities felt 
in after years in the form of a variety of pathological 
conditions. 


CHAPTER XXIX. 


LOCOMOTOR ATAXIA. 

(Tabes Dorsalis.) 

Locomotor ataxia is a disease of the sensory portion 
of the central nervous system, and is characterized ana¬ 
tomically by a sclerosis or fibrous-tissue formation in the 
posterior columns of the spinal cord, known as the col¬ 
umns of- Goll and Burdach. It has been established that 
this disease is always a late result of syphilis, and may 
occur in an individual that has to all appearances been 
cured of that infection, and in whom no symptoms what¬ 
soever have been present for as much as twenty-five 
years. 

Symptoms. 

1. Incipient stage: 

(1) Pain. Sharp, stabbing, called “lightning pains”; 

most common in the legs. 

(2) Ocular symptoms. Paralysis of external mus¬ 

cles of the eye, ptosis (drooping of upper 
lid), and Argyll Robertson pupil, in which the 
pupil loses its sensitiveness to light, but con¬ 
tinues to react to accommodation. 

(3) Difficulty in voiding urine. 

(4) Loss of patellar reflex (knee-jerk). 

Any or all of these symptoms may exist for several 
years, the patient remaining in a stationary condition. 

2. Ataxic stage. This develops gradually. “One of 
the first indications to the patient is inability to get 
about readily in the dark, or to maintain his equilibrium 

% 17 (257) 


258 


CLINICAL MEDICINE FOR NURSES. 


when washing his face with the eyes shut. When the 
patient stands with the feet together and the eyes closed, 
he sways and has difficulty in maintaining his position, 
and he may be quite unable to stand on one leg. He does 
not start off promptly at the word of command. On 
turning quickly he is apt to fall. He descends stairs with 
more difficulty than he ascends them. 

“Gradually the characteristic ataxic gait develops. The 
patient, as a rule, walks with a stick. The eyes are 
directed to the ground, the body is thrown forward, and 
the legs are wide apart. In walking the leg is thrown 
out violently, the foot is raised too high, and is brought 
down in a stamping manner, with the heel first, or the 
whole sole comes in contact with the ground. 

“Ultimately the patient may be unable to walk without 
the assistance of two canes. This gait is very character¬ 
istic, and unlike that seen in any other disease. The inco¬ 
ordination is not only in walking, but in the performance 
of other movements. It may early be noticed by a diffi¬ 
culty which the patient experiences when buttoning his 
collar, or when performing one of the ordinary routine 
acts of dressing. One of the most striking features of 
the disease is that with marked inco-ordination there is 
no loss of muscular power” (Osier). Shifting pains per¬ 
sist, and render many patients miserable. Attacks of 
severe pain referable to various organs of the body may 
occur. The so-called gastric crises are the most impor¬ 
tant—attacks of pain in the stomach, accompanied by 
nausea and vomiting. 

3. Paralytic Stage. After the ataxic stage has per¬ 
sisted for an indefinite time, the patient gradually loses 
the power of walking, and becomes bed-ridden or para¬ 
lyzed. In this stage the condition known as “surgical 


LOCOMOTOR ATAXIA. 


259 


kidney” (or ascending infection of the urinary tract) is 
apt to occur, or the patient may succumb to some infec¬ 
tion such as pneumonia or tuberculosis. 

Prognosis. Recovery is impossible, for certain fibres 
in the spinal cord are permanently destroyed. Arrest at 
any stage is often possible. 

Treatment. Antisyphilitic treatment energetically 
instituted is indicated in practically every case. Salvar- 
san combined with mercury gives the best results. Large 
doses of potassium iodide, formerly extensively used, 
are no longer considered advisable. The patient must be 
placed under the best possible hygienic surroundings, well 
fed, the avenues of elimination kept open, and particular 
attention paid to the skin, the nutrition of which is often 
interfered with. If bed-sores develop in these patients, 
they are apt to run a rapid and virulent course, and may 
prove fatal. 

Frankel has devised some special exercises for the re¬ 
education of co-ordination which are of value. The gen¬ 
eral treatment of locomotor ataxia, apart from the anti¬ 
syphilitic medication and Frankel’s exercises, is largely 
symptomatic, and in a disease characterized by so many 
symptoms, and extending over such a lengthy period of 
time, a recital of all methods employed would be too 
voluminous. 


CHAPTER XXX. 

DIABETES MELLITUS. 

Diabetes is a disease of nutrition, in which sugar (glu¬ 
cose) cannot be utilized in the usual way; hence it ap¬ 
pears in the blood, and is excreted in the urine (glyco¬ 
suria), the amount of which is greatly increased. 

Etiology. Heredity seems to play an important 
part. The disease is most frequent after 40 years of age, 
and, generally speaking, the earlier in life an individual is 
affected, the more severe is the type of the disease, and 
vice versa. Diabetes often develops after an infection 
or an injury. 

The lesion of diabetes is situated in the pancreas and 
manifests itself in the destruction of certain specialized 
cells, occurring in groups or islets, and known as the 
islands of Langerhans out of respect for their discoverer. 

Symptoms. The disease is gradual and insidious in 
its onset. Often the first symptom is sugar in the urine, 
which is accidentally discovered in the course of a 
routine examination, as, for instance, for life insurance. 
Other symptoms which are rather characteristic are: 

1. Excessive hunger. 

2. Excessive thirst. 

3. The passing of an excessively large amount of pale 
straw-colored urine—from 3 to 10 quarts in twenty-four 
'hours. 

4. Emaciation and increasing weakness. 

5. Crops of boils or carbuncles. 

6. Intense itching, often about the genitals. 

(260) 


DIABETES MELL1TUS. 


261 


7. The characteristic urinary findings: 

(a) Large amount of urine voided. 

( b ) High specific gravity—1.030 to 1.045. 

( c ) The presence of sugar. 

In untreated cases the disease progresses steadily, and a 
condition known as acidosis appears— i.e., the overloading 
of the body with acids. Substances known as beta-oxy- 
butyric acid, diacetic acid and. acetone appear in the urine. 
The appearance of these chemical compounds pave the 
way for the last act in the evolution of the disease. 

8. Diabetic coma. This may come on with weakness, 
a sweetish odor to the breath due to acetone, somnolence, 
and gradually developing unconsciousness, the patient 
dying in a few hours. Diabetic coma may begin with 
nausea, vomiting, headache, delirium, great distress, and 
dyspnea. Finally, there are cases in which without any 
previous warning the patient is seized with headache, a 
sense of intoxication, and rapidly passes into a deep coma 
which ends in death. 

Complications. The manifestations in the skin have 
been mentioned. It is a fact that diabetics show very 
little resistance to infection, and that in them trivial 
wounds and scratches become the starting-point for a 
spreading cellulitis, ending often in gangrene. Pulmon¬ 
ary tuberculosis is not infrequent, and is very fatal. 
Albuminuria is also of fairly common occurrence. 

Prognosis. In untreated cases of diabetes the out¬ 
look is absolutely bad. Under careful management much 
can be done for the patient, though it is not possible to 
speak of “cure” in connection with this disease. How¬ 
ever, in the mild and moderately severe types, judicious 
treatment will prolong life for years under very com¬ 
fortable conditions, but vigilance must never be relaxed, 


262 


CLINICAL MEDICINE FOR NURSES. 


for “the roots of sin are there/’ and if the patient insists 
on exceeding his dietetic limitations he soon pays for his 
indiscretion by a return of the old train of symptoms. 

Treatment. The treatment of no disease known to 
man is on a surer foundation than that of diabetes today. 
The brilliant results must be attributed to such men as 
Naunyn and Von Noorden abroad, F. M. Allen and E. P. 
Joslin in the United States, and Banting, Best and McLeod 
of the University of Toronto, Canada. These latter have, 
by their discovery of insulin, added the last word to the 
management of diabetes. 

It is impossible in the scope of a book such as this to 
take up in detail the treatment of diabetes. The general 
principles will be briefly and somewhat dogmatically laid 
down. Any nurse interested in the subject should pur¬ 
chase the “Diabetic Manual” of Dr. E. P. Joslin, of Bos¬ 
ton, published by Lea and Febiger, of Philadelphia, which 
is without doubt the best small book on diabetes ever 
written for nurse and layman, just as the same author’s 
large work on diabetes represents the best that has hith¬ 
erto been said on the subject. 

The essential defect in the diabetic lies in his inability 
to utilize starches and sugars, resulting in their elimina¬ 
tion in the urine. Hence, in order to overcome this de¬ 
fect, his diet must be so arranged that he will not be 
called upon to eat more carbohydrate foods than he can 
care for. At first sight, the elimination of all carbohy¬ 
drate would seem the logical method to pursue, but such 
a procedure would result in an absolutely unbalanced 
ration and would not better the patient’s ultimate condi¬ 
tion. The goal in the diet of the diabetic is to secure 
such a diet as will contain the greatest amount of carbo¬ 
hydrate he can take without the appearance of sugar in 


DIABETES MELLITUS. 


263 


the urine or without an increase over normal of the sugar 
in the blood, a sufficient amount of proteid and fat to meet 
his body needs, the whole totalling a number of calories 
adequate for the nourishment of the patient, that is, about 
forty calories per kilogram of body weight. 

The first thing to be done with any diabetic patient is 
to get him sugar-free and the second to determine his 
carbohydrate tolerance. Dr. Joslin has reduced these two 
procedures to their simplest form. He has a series of 
“Test Diets” and "Maintenance Diets” as seen in the 
accompanying table, together with another table of foods 
with their carbohydrate value. In actual practice these 
two tables are printed on opposite sides of a small card, 
published by Thos. Groome & Son, of Boston, and con¬ 
tain really the essentials of beginning treatment of every 
diabetic. 

The "Test Diets” are for use during the period in 
which the patient gradually becomes sugar-free. Through¬ 
out the entire period of determination of the final diet 
the patient can take, the twenty-four hour urine is saved 
and examined daily for sugar. On successive days the 
different test diets are given, going from TD 1 to TD 2 
and so on. If after TD 5 the patient is not sugar-free 
fasting can be employed, though in the light of most re¬ 
cent knowledge insulin would probably be resorted to. 

The maintenance diets are to be used as soon as the 
patient is sugar-free. It will be noted that they run in¬ 
versely to the test diets, for whereas in the latter the 
amount of carbohydrate is being steadily diminished, in 
the former it is being steadily increased. 

"If the urine becomes sugar-free as a result of test 
diet 5, the patient begins with Maintenance Diet C 1— 
PF 1. The actual articles of food representing the carbo- 


264 


CLINICAL MEDICINE FOR NURSES. 


Table I. 
Diabetic Diets. 


Diets with 

WHICH TO BE¬ 
COME SUGAR- 

FREE. 

Diet in Grams. 

Test Diets. 

■ 6 
o-y 

w 

d 

© 

s 

Ph 

-M 

a 

& 

W 

0) 

V» 

o 

73 

o 

C © 
*1 
|a 

*0 

d 

O 

1 

a 

a 

o 

T) 

tj a 

T3 0) 

© ja 

m 

c4 

ID 

(D 

fl 

P 

T. D. 1. 

T. D. 2. 

T. D. 3. 

T. D. 4. 

T. D. 5. 

189 

102 

64 

36 

15 

89 

58 

33 

27 

5 

15 

0 

0 

0 

0 

1247 

640 

388 

252 

80 

300 

300 

300 

300 

300 

300 

300 

300 

200 

50 


1 

1 


Maintenance 

Diets. 


Carbohydrate (C). 

C 1 — PF 1 

C 2 — PF 2 

C 3 —PF 3 

C 4 —PF 4 

C 5 —PF 5 

C 6 —PF 6 

C 7 —PF 7 

C 8 —PF 8 

C 9 —PF 9 

C 10—PF 10 

C 11—PF 11 

C 12—PF 12 

10 

22 

32 

42 

52 

63 

73 

83 

96 

107 

131 

155 

11 

13 

24 

29 

32 

43 

51 

60 

63 

64 

76 

80 

6 

18 

24 

39 

53 

65 

70 

88 

94 

94 

99 

99 

138 

302 

440 

635 

813 

1009 

1126 

1364 

1482 

1530 

1719 

1831 

300 

300 

600 

600 

600 

600 

600 

600 

600 

600 

600 

600 

100 

100 

200 

200 

200 

300 

300 

300 

300 

300 

300 

15 

30 

30 

30 

30 

30 

30 

30 

54* 

1 

1 

1 

2 

2 

2 

2 

2 


Food. 

Weight in Grams. 

Approximate Equivalent. 

Orange. 

.300. 

.. One and one-half, large size. 

5 per cent, vegetables 

.300. 

.. Three moderate portions. 

Skimmed milk . 

.480 . 

.. One pint, 16 ounces. 

Fish. 

. 120 . 

.. Two small portions. 

Potato . 

. 90. 

.. One moderate portion. 












































DIABETES MELLITUS. 


265 


Table I. 
Diabetic Diets. 





Test Diets. 





Potato. 

Bread. 

bo 

bO 

H 

Cream, 20 
Per cent. Fat. 

Bacon. 

Butter. 

Meat. 

Fish. 

Skimmed 

Milk. 

Name of 

Diet. 

240 

120 

60 

90 


... 

1 



90 

120 

180 

90 

90 

480 

300 

240 

120 

1 

2 

3 

4 

5 



Protein 

and Fat (PF). 





1 







1 



1 

60 

. , 


. . . 



• 2 



2 

60 


f # 

. , . 



3 



2 

60 

30 

, # 

. . . 



4 



2 

60 

30 

IS 

. . . 



5 



2 

90 

30 

15 

30 



6 



2 

90 

30 

15 

60 



7 



2 

90 

30 

30 

90 



8 



2 

120 

30 

30 

90 



9 



2 

120 

30 

30 

90 



10 

m 


2 

120 

30 

30 

120 



11 

240 


2 

120 

30 

30 

120 



12 


Food. Weight in Grams. Approximate Equivalent. 


Bread . 

.90. 


Oatmeal, dry weight .... 

.30. 


Cream . 

.60. 

.Four tablespoonsful. 

Bacon . 

....30. 


Butter . 

.30. 

































































Table II. —Diabetic Diets. 

Water, Clear Broths, Coffee, Tea, Cocoa Shells and. Cracked Cocoa can be taken 
without allowance for food content. 


Foods Arranged Approximately According to Content of Carbohydrates. 


1 to 3% 

3 to 5% 

10% 

15% 

20% 

^ Lettuce 

Tomatoes 

String beans 

Green peas 

Potatoes 

Cucumbers 

Brussels 

Pumpkin 

Artichokes 

Shell beans 

s Spinach 

sprouts 

Turnip 

Parsnips 

Baked beans 

| Asparagus 

Water-cress 

Kohl-rabi 

Canned lima 

Green corn 

Rhubarb 
^ Endive 
° Marrow 
^ Sorrel 
£ Sauerkraut 
^ Beet greens 
Dandelion 

S greens 

S Swiss chard 
•S Celery 

§> Mushrooms 
<*> 

Sea kale 

Okra 

Cauliflower 

Egg-plant 

Cabbage 

Radishes 

Leeks 

String beans, 
canned 
Broccoli 
Artichoke®, 
canned 

Squash 

Beets 

Carrots 

Onions 

Green peas, 
canned 

beans 

Boiled rice 
Boiled 
macaroni 

Ripe olives (20 per cent, fat) 
Grapefruit 

00 

•<>> 

Watermelons 

Strawberries 

Lemons 

Cranberries 

Peaches 

Pineapple 

Blackberries 

Gooseberries 

Orange® 

Raspberries 

Currants 

Apricots 

Pears 

Apples 

Huckleberries 

Blueberries 

Cherries 

Plums 

Bananas 

Prunes 


Reckon average carbohydrate in 5 per cent, vegetable as 3 per cent. 
Of 10 per cent, vegetables as 6 per cent. 


1 Gm. protein = 4 calories. 

1 Gm. carbohydrate = 4 calories. 

1 Gm. fat = 9 calories. 

G.25 Gms. protein = 1 Gm. nitrogen. 


1 kilogram = 2.2 pounds. 

30 grams (Gm.) or cubic centi¬ 
meters (c.c.) = 1 ounce. 

A patient “at rest’’ requires 25 
calories per kilogram. 


30 grams (1 ounce). Carbohydrates Protein Fat Calories 
Contain approximately Gm. Gm. Gm. 

Oatmeal, dry weight . 20 5 2 118 

Shredded wheat . 23 3 0 104 

Uneeda biscuits, two . 10 1 1 53 

Cream, 40 per cent. 1 - 1 12 116 

Cream, 20 per cent. 1 1 6 62 

Milk . 1.5 1 1 19 

Brazil nuts . 2 5 20' 208 

Oysters, six . 4 6 1 49 

Meat (cooked, lean) . 0 8 5 77 

Chicken (cooked) . 0 8 3 59 

Bacon . 0 5 15 155 

Cheese . 0 8 11, 131 

Egg (one) . 0 6 6 78 

Vegetables, 5 per cent, group . 1 0.5 O 6 

Vegetables, 10 per cent, group .... 2 0.5 0 10 

Potato . 6 1 O 28 

Bread . 18 3 0 84 

Butter . 0 0 25 225 

Oil . 0 0 30 270 

Fish, cod, haddock (cooked) . 0 6 O 24 

Broth . 0 0.7 0 3 


( 266 ) 










































DIABETES MELLITUS. 


267 


hydrate in the diet for the first day are given under the 
heading of carbohydrate, for convenience described as C, 
C 2, C 3, etc. The articles referred to under protein and 
fat are under the heading which, for the same reason, is 
described as PF 1, PF 2, PF 3, etc. Certain cases of 
diabetes can proceed steadily day by day from C 1—PF 1 
to C 12—PF 12, without showing sugar. If sugar does 
appear in the urine the diet is dropped back two days in 
the carbohydrate group until the urine becomes sugar-free, 
and is then advanced in the protein and fat group until 
sufficient calories are obtained. Thus, if sugar appears 
on C 7—PF 7, the diet prescribed would be that included 
in C 5—PF 7 and thereafter progression would be made 
in the PF group until twenty-five or thirty calories and 
a gram of protein per kilogram of body weight per twenty- 
four hours were furnished the patient. 

“Occasionally the patient becomes- sugar-free on Test 
'Diet 2, 3 or 4. It is then unnecessary to begin with Main¬ 
tenance Diet C 1—PF 1, but instead with a maintenance 
diet which contains a value for carbohydrate similar to 
that of the test diet upon which the patient became sugar- 
free” (Reginald Fitz). 

Thus by care, a little close application and the use of 
these excellent tables, the carbohydrate tolerance of the 
patient can be determined. While approximate equiva¬ 
lents of grams in ordinary measures such as “portions,” 
“slices,” “ounces” are given, it is far preferable to buy a 
pair of diabetic scales which cost $10.00 and which insure 
accuracy. The carbohydrate tolerance having been deter¬ 
mined, it is attempted to give the patient a sufficient num¬ 
ber of calories to meet his nutritional needs without over¬ 
feeding protein or fat, for to 1 do so will often bring about 
digestive disturbances, and furthermore as both protein 


268 


CLINICAL MEDICINE FOR NURSES. 


and fat are in part convertible into carbohydrate, will tend 
to overstep the limits of carbohydrate tolerance. If a 
satisfactory diet can be secured, insuring the maintenance 
of weight and strength of the patient, the object has been 
attained and watchfulness is all that is necessary. Foods 
are varied to suit the taste and to avoid too great 
monotony. The urine is examined daily and the patient 
goes about his business, a diabetic to be sure, but feeling 
no ill effects as long as he adheres rigorously to his dietary 
limitations and does not overstep his carbohydrate toler¬ 
ance. A certain number of patients will be able to reach 
this goal. A large proportion, however, cannot assimilate 
enough carbohydrate to meet their bodily needs. In these 
cases recourse is now had to insulin. 

Insulin, an extract of the islands of Langerhans, was 
first used on a human diabetic at the University of 
Toronto, January 10, 1922. Its success is the result of 
the brilliant conception of Dr. F. G. Banting, ably seconded 
by his friend, C. H. Best, and by J. J. R. McLeod, profes¬ 
sors of Physiology in the University of Toronto. 

Insulin enables the diabetic to metabolize more 
carbohydrate and therefore raises his carbohydrate 
tolerance. It consequently permits those who form¬ 
erly could not assimilate a maintenance diet of suf¬ 
ficient caloric value for their body needs to utilize to the 
full a satisfactory diet and thus to put on weight and 
strength. It is one of the most brilliant discoveries of 
modem medicine. There are, however, a few facts in 
connection with insulin which must be very plainly 
stressed. 

1. Insulin does not cure diabetes. Insulin simply en¬ 
ables the diabetic to metabolize more carbohydrate with¬ 
out showing glycosuria. 


269 


DIABETES MELLITUS. 

2. Insulin does not do away with the dietetic treatment 
of diabetes. On the contrary, the best results with insulin 
will be obtained only where strict attention is paid to all 
details of the diet, and when only enough insulin is given 
to enable the patient to metabolize sufficient carbohydrate 
to be able to take an adequate maintenance diet. 

3. Insulin should not be used in every case of diabetes, 
but only in those cases that cannot take an adequate main¬ 
tenance diet and remain sugar-free. 

4. Insulin if given carelessly is dangerous. It markedly 
reduces the blood sugar and when this goes below 0.080 
gram per 100 c.c. of blood, symptoms of hypoglycemia set 
in, which are characteristic and are known as an “insulin 
reaction.” These may set in a few minutes after adminis¬ 
tration and are: 

Hunger and tremor. 

Nervousness and weakness. 

Pallor—flushing of the face, dilated pupils. 

Stupor and unconsciousness. 

The treatment is simple and effective. It consists in the 
prompt administration of any carbohydrate out of which 
glucose can be quickly formed. 

Orange juice, 20 to 50 c.c. 

Two or three pieces of sugar or candy. 

Honey or cane syrup. 

A solution of glucose, 5 to 20 per cent. 

Recovery is usually prompt and after-effects nil. 

The Strength of Insulin. It has been estimated that one 
unit of insulin will allow the patient to assimilate two 
grams of glucose. The patient’s carbohydrate tolerance 
being known, and it being determined how much more 
glucose it is desired to have that patient assimilate, the 
calculation of the number of units of insulin to be given 


270 


CLINICAL MEDICINE FOR NURSES. 


can easily be made. It is wise to start with small doses of 
insulin and gradually to work up until the patient is taking 
enough to enable him to care for a satisfactorily balanced 
diet. 

Insulin is given hypodermically, usually two or three 
times daily from fifteen to thirty minutes before meals. 
It is put up in small vials containing a given number of 
units per c.c. so that the calculation of the dose is easy. 

In cases of diabetic coma insulin gives brilliant results, 
being then administered in large doses subcutaneously or 
intravenously. Details are not given here, as the nurse 
will never be called upon to deal personally with this 
condition. 

Experience gathered so far tends to show that the pa¬ 
tient that needs insulin at all needs it permanently. Omis¬ 
sion of insulin is fraught with grave dangers. We can¬ 
not do better than to quote Dr. Joslin: 

“Too much emphasis cannot be laid upon the danger of 
continuing the high diet when insulin is discarded. The 
foundations for the increased diet are certainly removed 
when insulin is omitted. . . . With increased diets due 
to insulin patients are walking on insulin stilts. The 
longer the stilts, the greater the danger of a fall when they 
are taken away. In this diabetic game one is treating pa¬ 
tients for years and the closer one keeps to the ground, 
the better.” 

The amount of insulin to be given varies with each 
individual case and no general rules can be given. The 
amount of carbohydrate it is desired to give must be es¬ 
timated by the physician and enough insulin given to allow 
assimilation of the number of grams of glucose existing in 
the total carbohydrate intake desired, minus the carbo- 
hydrate tolerance of the patient. To illustrate: a patient 


DIABETES MELLITUS. 


271 


is found to have a carbohydrate tolerance of 80 grams 
It is desired to give him 160 grams. Therefore, enough 
insulin should be given to allow the assimilation of 80 
grams (160 to 80). If the assaying power of one unit of 
insulin be taken to be 2 grams of glucose the patient 
should receive 1 40 units every twenty-four hours. 

Since the introduction of insulin diabetics have been 
rendered far better surgical risks. Formerly the sugar- 
saturated tissues were fertile soil for infection and any 
surgical procedure in a diabetic was looked upon with 
dread and postponed as long as possible. Now major 
operations can be performed with relative impunity. Dia¬ 
betics having also pulmonary tuberculosis, a frequent and 
formerly a uniformly fatal complication (the dietetic 
treatment of the two diseases being diametrically opposed), 
now have a far better chance for improvement, since with 
insulin their food intake can be so markedly increased. 
Acidosis and diabetic coma are disappearing in the prop¬ 
erly treated cases, and many of the untreated cases are 
being saved from certain death. It is difficult to over¬ 
estimate the value of insulin but it must ever be remem¬ 
bered that it is only in close adherence to the fundamental 
and well-known dietetic principles, in the careful and 
painstaking instruction of patients and in the judicious 
dosage of insulin that its best and most brilliant results 
can be obtained. 


CHAPTER XXXI. 

THE BLOOD. 

The blood is the nutritive medium of the body, dis¬ 
tributes food and oxygen to all the tissues, and takes 
from them waste products to be delivered to the organs 
of elimination. It comprises about one-thirteenth of the 
body weight. 

The blood is composed of a liquid portion, blood- 
plasma, in which are floating the cellular elements or cor¬ 
puscles of the blood: 

1. Red blood-cells—erythrocytes. 

2. White blood-cells—leukocytes. 

3. Blood-platelets. 

Plasma. Normally, when free from corpuscles, plasma 
in thin layers is clear and colorless. When seen in thicker 
layers it has a faint yellow tinge. Blood upon escaping 
from the blood-vessels usually clots. The clot in its for¬ 
mation shrinks and squeezes out a fluid having a slightly 
yellow tinge. This is known as blood-serum. It may be 
said that plasma is the liquid part of blood before clot¬ 
ting, and serum the liquid part of the blood after clotting. 
In the blood-serum are contained many of the substances 
that figure so largely in the different phases of immunity. 
These will be touched on in the chapter on “Immunity.” 

Clotting. One of the most remarkable properties of 
blood is its power to coagulate or clot immediately or 
very shortly after escaping from the vessel. This power 
of clotting saves the life of each one of us countless 
times, for were it not for the blood-clot, we would all 
(272) 


THE BLOOD. 


273 


die of hemorrhage from the most trivial injury. There 
are indeed individuals known as haemophiliacs, or bleed¬ 
ers, whose blood clots very slowly, if at all, and who fre¬ 
quently bleed to death from some very trifling cut or 
operation. 

“The essential part of the blood-clot is the fibrin. 
Fibrin is an insoluble proteid which is absent from nor¬ 
mal blood. In blood that has been shed—and, under 
certain conditions, in blood while still in the blood-ves¬ 
sels—this fibrin is precipitated, if the word may be used, 
in the form of an exceedingly fine network of delicate 
threads, which permeates the whole mass of blood, and 
gives the clot its jelly-like character. The shrinking of 
the threads causes the subsequent contraction of the clot. 

“If the blood has not been shaken in the act of clotting, 
almost all the red corpuscles are caught in the fine fibrin 
meshwork, and as the clot shrinks these corpuscles are 
held more firmly, only the clear liquid of the blood being 
squeezed out, so that it is possible to get specimens of 
serum containing few or no red corpuscles. The leu¬ 
kocytes, on the contrary, although they are also caught 
‘at first in the forming meshwork of fibrin, may readily 
pass out into the serum in the later stages of clotting, on 
account of their power of ameboid movement (see chap¬ 
ter on Immunity). If the blood has been agitated during 
the process of clotting, the delicate network will be 
broken in places, and the serum will be more or less 
bloody—that is, it will contain numerous red corpuscles. 

“If during the time of clotting the blood is vigorously 
whipped with a bundle of fine rods, all the fibrin will be 
deposited as a stringy mass upon the whip, and the re¬ 
maining liquid part will consist of serum plus the blood- 
corpuscles. Blood which has been whipped in this way 

18 


274 


CLINICAL MEDICINE FOR NURSES. 


is known as ^efibrinated’ blood. It resembles normal 
blood in appearance, but is different in its composition: 
it cannot clot again” (An American Textbook of 
Physiology). 

The cellular elements of the blood. 

1. Red Cells or Erythrocytes. These are small bi-con¬ 
cave disks, practically round when normal, and having 
in the fresh state a yellowish color when looked at under 
the microscope. They are very numerous, there being in 
men about 5,000,000 to the cubic millimeter, and in 
women about 4,500,000. A normal red cell is never 
nucleated. 

In anemia from any cause, the red cells are reduced in 
number and changed in character—to what extent de¬ 
pends upon the severity of the anemia. The lowest red 
blood-count on record is 143,000 per cubic millimeter. 

The following changes may take place in red cells as 
a result of severe anemia: 

(a) Great pallor, due to deficient amount of hemo¬ 

globin. 

( b ) Poikilocytosis, or irregularity in outline. 

(c) Nucleation (normoblasts), due to the throwing 

into the circulation by the bone-marrow of 
young immature forms, in order to supply the 
crying need for blood-cells. 

( d ) Appearance of large nucleated red cells (me- 

galoblasts), representing still more immature 
forms thrown out when the body’s need for 
new cells is most urgent. 

(e) “Stippling” of red cells—a form of degeneration. 

2. White Cells or Leukocytes. These cells are far less 
numerous than the red cells, a normal leukocyte count 
showing from 4000 to 7000 per cubic millimeter. There 


THE BLOOD. 


275 


are several varieties of leukocytes. The following table 
gives the main varieties and the approximate percentage 
in normal blood: 

Per cent. 


Polymorphonuclear neutrophile . 65 

Small lymphocyte. 20 

Large lymphocyte. 10 

Eosinophile. 3 

Basophile (mast-cell) . 2 


100 

The leukocytes, as mentioned above, are capable of 
motion by means of their power of ameboid movement, 
and are very active as scavengers of the body, and as 
faking a prominent part in the fight against infection. 
This function is referred to in the chapter on Immunity. 

Leukocytosis. By leukocytosis is meant an increase 
in the number of leukocytes in the blood. All leukocytosis 
is pathological— i.e., is called forth by the presence of an 
enemy most frequently in the form of some infection. 
The exception to this rule lies in those blood diseases 
known as the leukemias, where, owing to an abnormality 
of the blood-forming organs, especially the spleen, a vast 
number of immature leukocytes are flung into the cir¬ 
culation. Leukocytosis occurs-in all infections and in¬ 
fectious diseases except: 

1. Typhoid fever. 

2. Uncomplicated tuberculosis. 

3. Malaria. 

4. Influenza. 

5. Measles. 

6. Mumps. 

7. Leprosy. 

The usual count when a moderate leukocytosis exists 
is from 15,000 to 30,000. Occasionally the count will be 







276 


CLINICAL MEDICINE FOR NURSES. 


as high as 50,000 or 75,000. In the leukemias the white 
cells may number 500,000 to the cubic millimeter, and 
even more. 

The presence or absence of a leukocytosis is often of 
great value in diagnosis, and the nurse should appreciate 
its importance and learn to understand its significance in 
conditions where the count is frequently made. The fol¬ 
lowing rules may prove of aid: 

1. If the infection is severe, and the patient’s resist¬ 
ance good, leukocytosis is early, marked, and persistent. 

2. If infection and resistance are both less marked, 
but fairly well proportioned one to the other, leukocytosis 
still occurs, but comes later, is less in degree, and ceases 
more quickly. 

3. If the infection is one of unusual virulence, as in 
the so-called “fulminating” cases of sepsis, diphtheria, or 
pneumonia, no leukocytosis occurs. 

4. Occasionally when the infection is unusually mild, 
and the resistance unusually good, there may be little 
or no leukocytosis. 

Hemoglobin. The hemoglobin is the coloring mat¬ 
ter of the red cells, and is the substance to which the 
blood owes its red color. A chemical change in the 
hemoglobin in combination with each red cell is respon¬ 
sible for the fact that arterial blood is bright red, and 
venous blood a deep crimson. (See chapter on the 
Circulation.) 

Hemoglobin estimations are very frequently made, the 
test being the most simple of any applied to the blood. 
Normal hemoglobin content ranges from 90 per cent, to 
110 per cent, on the scale with which the blood under 
examination is compared, and in all probability treat- 


THE BLOOD. 


277 


ment would rarely be instituted with a normal red cell 
count and hemoglobin 80 per cent, or over. 

Hemoglobin varies pathologically in three ways: 

1. Proportionately to the loss in red cells— i.e., with a 
red cell count of 3,750,000 (25 per cent, less than nor¬ 
mal) a hemoglobin reading of approximately 75 per cent. 

2. Relatively high as compared with the number of 
red cells. This condition occurs in all anemias of the 
pernicious type— e.g., a red cell count of 2,000,000 (a loss 
of almost 60 per cent, of red cells), and a hemoglobin 
reading of approximately 55 per cent. (In order to be 
in proportion to the red cell loss, the hemoglobin reading 
should be in the neighborhood of 40 per cent.) 

3. Actually low and relatively low as compared to the 
number of red cells. This relationship occurs particu¬ 
larly in chlorosis—that anemia of young girls that seems 
to consist almost, entirely in a hemoglobin deficiency— 
e.g., red cell count 4,000,000, hemoglobin 35 per cent. 

In addition to estimating the percentage of hemoglobin, 
and the number of red and white cells, a differential 
white cell count is often done in order to determine 
whether there is any change in the percentage of the 
various types of leukocytes, as such changes are often of 
aid in diagnosis. No attempt will be made to dwell upon 
results obtained from differential white cell counts, as 
the nurse is in no wise concerned with them. 


CHAPTER XXXII. 


PERNICIOUS ANEMIA AND LEUKEMIA. 

Pernicious anemia is “a chronic and usually fatal 
disease of unknown origin, producing, especially in elderly 
men, paroxysms of intense anemia, and usually degenera¬ 
tion of the spinal cord” (Cabot). 

The cause of pernicious anemia is as yet unknown. 

Symptoms. A characteristic of pernicious anemia is 
its insidious onset. General weakness is complained of 
in every case. The early cases are extremely difficult to 
recognize, but when the condition is moderately advanced 
the patient’s color is very suggestive. A yellowish pal¬ 
lor is present, the patient having a dead, waxy tinge, dif¬ 
ferent from that seen in other forms of anemia. It is 
a color that must be seen to be appreciated; no amount 
of description can do it full justice. In connection with 
general weakness the patient also complains of other symp¬ 
toms, some of which are characteristic of any severe 
anemia, others of which point more or less directly to 
the pernicious type. 

Those symptoms present in any severe anemia are: 
dyspnea, palpitation, headache, vertigo, and less fre¬ 
quently, edema. 

Those symptoms more or less characteristic of perni¬ 
cious anemia are: 

1. Gastrointestinal attacks or “crises”—paroxysms of 
severe abdominal pain, practically uninfluenced by treat¬ 
ment, passing off at the end of a variable length of time, 
and often followed by a period of improvement. 

(278) 


PERNICIOUS ANEMIA AND LEUKEMIA. 279 


2. Diarrhea. Continuous or paroxysmal. 

3. Symptoms suggestive of tabes dorsalis (locomotor 
ataxia) (q-v.). 

Usually there is but slight loss of weight as compared 
with the general weakness. The most characteristic symp¬ 
toms of .pernicious anemia are to be found in 

The hlood: 

The total quantity of blood is lessened. 

Blood-pressure is extremely low. 

On pricking the finger the drop of blood may look quite 
red, but its watery condition is at once apparent. The red 
cells are usually found to be below 2.000,000 to the cubic 
millimeter (normal being from 4,500,000 to 5,000,000). 
The hemoglobin may be 50 per cent, of normal, while the 
red cells may be but 40 or 30 per cent, of normal. This 
condition is characteristic of pernicious anemia, and is the 
result of nature’s effort, in view of the very great destruc¬ 
tion of red cells, to supply each remaining cell with as 
great a percentage of hemoglobin as possible. In addi¬ 
tion, it may merely be mentioned in passing that the out¬ 
lines of the red cells are irregular instead of being smooth 
and round, that the average size of the red cells is in¬ 
creased, due to young, immature forms being cast into the 
circulation to make up for the loss in cells, and that red 
cells containing nuclei are found. 

The course of the disease is characterized by periods of 
marked improvement followed by periods of increase in 
all symptoms. The blood-picture varies with the general 
symptoms, sometimes improving to a remarkable degree, 
only to grow worse again. The outlook for permanent 
recovery is bad, but if the patient reacts satisfactorily to 
treatment, life may be maintained for several years. The 


280 


CLINICAL MEDICINE FOR NURSES. 


blood-picture rarely, if ever, reaches normal, but periods 
of improvement may last from three months to two years. 

Treatment. Rest in bed for a time, fresh air, food in 
abundance are, of course, indicated. The general manage¬ 
ment is very similar to that employed in pulmonary tuber¬ 
culosis ( q.v .). Blood transfusions prove most valuable 
and by their use life can be indefinitely prolonged and the 
patient relatively freed from a condition of hopeless in¬ 
validism. Transfusions have practically supplanted all 
drug treatment. 

Leukemia. This is a disease of one of the blood- 
forming organs, especially the bone-marrow. Nothing is 
known as to its causation. The condition is rare. 

There are two main classes: 

1. Myeloid. 

2. Lymphoid. 

1. Myeloid. Symptoms: 

(1) Enlarged, spleen. Usually reaches the navel; 

may extend into the pelvis. 

(2) Dyspnea. 

(3) Intestinal disturbances, due to pressure from 

enlarged spleen, and to dragging of the spleen 
on its ligaments. 

(4) General loss of strength. 

(5) Blood-picture. Leukocytes enormously in¬ 

creased in numbers. Usually 300,000 to 
1,500,000 per cubic millimeter (normal 4000 
to 7000). Abnormal forms known as mye¬ 
locytes present in large numbers. Moderate 
anemia. 


PERNICIOUS ANEMIA AND LEUKEMIA. 281 

2. Lymphoid. Symptoms: 

May be acute and begin with weakness, fever and 
hemorrhages from various portions of the body. 
May be glandular enlargement. 

Dyspnea. Spleen enlarged—less so than in myeloid 
form, but almost always present. 

Blood-picture. Leukocytes markedly increased, 
averaging about 180,000 per cubic millimeter and 
consisting practically entirely of lymphocytes. 

Course. These two forms of leukemia are generally 
chronic from the start, and usually end fatally, though, 
as in the case of pernicious anemia, there are frequently 
extended periods of improvement. 

Treatment. X-ray treatment at the hand of an ex¬ 
perienced operator has given the best results. No drug 
exerts any appreciable effect on the course of the malady. 


CHAPTER XXXIII. 

EXOPHTHALMIC GOITRE. 

(Graves’s Disease.) 

Exophthalmic goitre is a disturbance of nutrition due 
to a disordered condition of the thyroid gland. This 
gland, like the adrenal glands, the ovaries, etc., furnishes 
to the body what is known as an “internal secretion”— 
i.e., a secretion that is not given off through a duct, but 
that comes off from the body of the thyroid itself and 
spreads about through the tissues. The nature of this 
secretion is not well understood, but its presence is essen¬ 
tial to life. It is generally believed that exophthalmic 
goitre is due to an excessive secretion on the part of the 
thyroid gland, the evidence for this belief resting mainly 
on two facts: 

1. The conditions of myxedema and cretinism, which 
are positively known to be due to insufficient thyroid 
secretion, present a picture which is diametrically oppo¬ 
site to that found in exophthalmic goitre. 

2. Cases of exophthalmic goitre are almost invariably 
made worse by the administration of thyroid extract, 
which contains the active principle of the secretion of 
that gland. 

Exophthalmic goitre is not a rare condition, and is 
assuredly met with, especially in its milder forms, more 
frequently than is generally believed to be the case. The 
earlier forms are so like mild cases of neurasthenia that 
this diagnosis is more frequently made. 

Women are more frequently affected than men in the 
proportion of 8:1. The disease is one of early and 
(282) 


EXOPHTHALMIC GOITRE. 


283 


middle adult life, occurring usually between the ages of 
16 and 40. As predisposing causes are mentioned emo¬ 
tional shocks and worry, though it is probable that in 
these cases the disease was latent, and that its symptoms 
began to show themselves after bodily, and especially 
nervous, resistance had become lowered. The actual 
cause of the disease is unknown. 

Symptoms. There are five characteristic symptoms 
of exophthalmic goitre: 

1. Goitre. 

2. Exophthalmos—bulging of the eyeballs. 

3. Tachycardia—rapid heart action. 

4. Tremor. 

5. Nervousness. 

The onset of the disease is very gradual, the patient 
usually complaining for some weeks or months of in¬ 
creasing nervousness, palpitation, shortness of breath, 
and inability to perform ordinary duties without undue 
fatigue. 

In a well-developed typical case the neck is prominent 
from the swelling of the thyroid gland, the eyes are star¬ 
ing and bulge perceptibly, the heart action is rapid— 
from 120 to 150 per minute—there is palpitation accom¬ 
panied often by a choking sensation, and slight exertion 
brings on marked shortness of breath. When the hands 
are held out and the fingers spread apart as far as pos¬ 
sible a very fine tremor is observed in them, and as a 
rule the hands sweat profusely. There is intense nerv¬ 
ousness ; the patient starts at the slightest sound. There 
is inability to concentrate the attention on anything for 
any length of time; and the patient’s spirits are poor. 
The appetite is bad, the tongue is coated, and constipa¬ 
tion is frequent. There is almost always marked loss of 


284 CLINICAL MEDICINE FOR NURSES. 


weight and insomnia. At times! there is a low grade of 
fever, but this is not a prominent symptom, save in the 
most severe cases. The basal metabolism shows a marked 
and constant increase over normal. 

Some of the classical symptoms of exophthalmic goitre 
are very often absent, notably that of goitre. The protru¬ 
sion of the eyes may be extremely slight but cases are on 
record in which it has been so marked that the eyes could 
not be closed, and eventually the eyeballs sloughed away. 

Tachycardia, tremor, nervousness, with slightly staring 
eyes are the symptoms most commonly noted. 

Prognosis. It has been said that exophthalmic 
goitre is “a disease from which patients never recover and 
never die.” This is hardly true —it is better to say that 
“few recover and some die.” Recovery in the fullest 
sense of the word is not frequent, the best results usu¬ 
ally being the restoration of the patient to a condition 
which enables her to lead a happy and useful life, but one 
during which she must be ever careful not to overdo, and 
during which she must take longer or shorter periods of 
rest in order to tide over the times when the thyroid 
again begins secreting too actively. 

Treatment. As far as the general management is 
concerned, a routine is indicated which strongly re¬ 
sembles that advocated for cases of early pulmonary 
tuberculosis (for details see chapter on Tuberculosis), 
consisting in rest in the open air and abundant, nutri¬ 
tious, and easily digestible food. Nervousness is gen¬ 
erally best dealt with by means of continued rest, warm 
baths at night, and the administration of full doses of the 
bromides when necessary. It is not considered good 
practice to give morphia or any of the preparations of 
opium to these patients. 


EXOPHTHALMIC GOITRE. 


285 


Iodine is a drug that sometimes helps these patients, 
and sometimes seems to make the condition worse. 
When used it is usually given in the form of potassium 
iodide and the syrup of the iodide of iron. Iron in some 
form is often given, as there is usually a moderate de¬ 
gree of anemia. 

The use of extracts of the thymus gland, and the use 
of thyroidectin, which is a substance made from the 
blood of sheep whose thyroid glands have been removed, 
have benefited some cases, while in the majority of in¬ 
stances they have failed. 

Surgical Treatment. Surgery has been of greater 
benefit to cases of exophthalmic goitre than has medical 
treatment. Two main surgical procedures are in use: 

1. Resection of a portion of the gland (usually not 
over two-thirds). 

2. Ligation of two or three of the four thyroid arteries 
in the hope of lessening the activity of the gland by limit¬ 
ing its blood-supply. 

Probably the best treatment for a case of exophthalmic 
goitre is surgery in the hands of an expert, together with 
careful previous and subsequent general management 
on the part of the general practitioner. 


CHAPTER XXXIV 


IMMUNITY. 

Immunity is defined as “exemption from disease,” or 
that condition of the body which enables it to resist in¬ 
fection. Immunity and infection, though opposites, are 
so intertwined that mention cannot be made of one with¬ 
out reference to the other. 

Immunity can be classified as follows: 

1. Natural immunity. Thus, the human race is nat¬ 
urally immune to chicken cholera, and animals are 
naturally immune to measles. 

2. Acquired immunity. Thus, one attack of typhoid 
fever usually renders an individual immune to that 
disease. 

A certain amount of immunity may be acquired 
toward a particular disease by its frequent occurrence. 
When syphilis first appeared among Europeans, its rav¬ 
ages were frightful; but within fifty years, as a result 
of the countless number of cases that appeared, in¬ 
dividuals developed a relative immunity to the disease, 
and as a result its manifestations were not as terrible. 

When an individual is attacked by an infection, the 
defensive resources, or immunizing forces of the body, 
are called upon to do their part in repelling the invader. 
The stronghold of the defensive resources of the body is 
the blood. Certain cells of the blood play an active part 
in resisting infection, and many substances present in 
the blood-serum play their part in safeguarding the 
organism. 

( 286 ) 


IMMUNITY. 


287 


Phagocytosis. By this is meant the power of the white 
blood-cells to ingest, kill, and digest bacteria. Elie 
Metchnikoff, of Paris, is the man to whom science owes 
an unpayable debt for his labor in demonstrating the act 
and consequences of phagocytosis. It is known that the 
leukocytes are capable of motion by projecting a portion 
of their body in the shape of a long finger-like process. 
The rest of the body of the leukocyte is then drawn up 
to the finger-like projection, and thus the leukocyte 
moves. This is known as “ameboid” movement. When 
an infection exists, leukocytes at once come to the battle¬ 
ground, and a struggle ensues between them on the one 
hand, and the bacteria on the other. The leukocytes by 
their power of ameboid movement surround one or more 
bacteria, engulf them, and digest them. This can be 
observed under the microscope, the bacteria being seen 
to be engulfed, to grow less and less distinct within the 
body of the leukocyte, and finally to become wholly in¬ 
visible. If the infection is not of excessive virulence, and 
if the leukocytes are healthy and plentiful, the body wins 
the fight against the bacteria and recovery ensues. This 
is why it is always a good sign in an acute infection, such 
as lobar pneumonia or appendicitis, to have the blood 
show a high leukocyte count. If, however, the infection 
is very virulent, and the body defenses inadequate, no 
leukocytosis results and death ensues. 

Metchnikoff has shown that acquired immunity is 
largely due to stimulated phagocytosis. This is true 
whether the immunity is due to one attack of the disease 
or to vaccination. A rabbit which has been artificially 
immunized to anthrax shows a more marked phagocytosis 
on inoculation with a virulent culture than does a rabbit 
that has not been artificially immunized. 


288 


CLINICAL MEDICINE FOR NURSES. 


In the blood-serum are found many substances that 
play a role in the production of immunity. Among these 
may be mentioned: 

1. Precipitins. 

2. Agglutinins. Substances that cause bacteria to 
clump, and upon whose presence is based the Widal re¬ 
action, so valuable in the diagnosis of typhoid fever. 

3. Opsonins. Substances that, as it were, prepare and 
make ready bacteria, so that they can more readily be 
engulfed by the leukocytes in the process of phagocytosis. 

The theories of the mechanism of immunity are ex¬ 
tremely complex, and no attempt will be made to 
describe them here. Paul Ehrlich, of Berlin, has elab¬ 
orated the chief among them, his famous “side chain” 
theory of immunity, which in brief is as follows: A cell 
possesses normally certain defensive forces or receptors 
which will unite with a certain amount of toxin and 
neutralize it, thus protecting the cell. When a cell is 
threatened with attack by a toxin, it is stimulated to the 
production of other receptors, or “side chains,” and im¬ 
munity comes about when there is such an overproduc¬ 
tion of these side chains that there are more than enough 
to neutralize every bit of toxin that is attacking. 

Acquired immunity may be: 

1. Active. 

2. Passive. 

In specific treatment of various infections it is sought 
in some cases to produce an active immunity, in others a 
passive immunity. 

By an active immunity is meant that the body, stimu¬ 
lated by the infecting bacteria, or by the injection of 
those same bacteria killed (i.e., a vaccine), manufactures 
its own resisting forces, brings up its own reserves, and 


IMMUNITY. 


289 


actively fights its own battle. Vaccination against typhoid 
fever is a good example of the production of an active 
immunity, for, as a result of the injection of a certain 
number of killed typhoid bacilli, the body is stimulated to 
such an overproduction of receptors for typhoid toxin 
that it can resist infection with live typhoid bacilli, and 
not become ill with the disease. 

By passive immunity is meant that the body is sup¬ 
plied from outside with its means of defense, ready to 
use, and requiring no effort at all on the part of the 
individual. 

The best example of the production of a passive im¬ 
munity is to be found in the antitoxin treatment of diph¬ 
theria. Here, a certain amount of antitoxin secured from 
another artificially immunized animal (the horse) is in¬ 
jected, and at once is able to neutralize the diphtheria 
toxin circulating in the patient’s blood. This neutraliza¬ 
tion goes on with no effort whatsoever on the part of 
the patient, whose role is merely passive. This form of 
immunity can be used with success only in those diseases 
that are purely toxic, i.e., in which the infecting bacteria 
themselves do practically no harm, but only the poisons 
liberated by those bacteria. Hence, the use of antitoxic 
sera, while giving brilliant results in purely toxic dis¬ 
eases such as diphtheria and tetanus, have unfortunately 
but a very limited range of application. 

To quote Vaughan: “Now we have the great problem 
of infection and immunity fairly before us. It is a con¬ 
test between bacteria and body-cells, and . . . they 

are armed with similar weapons. The bacterial cells 
have their enzymes, poisons, and toxins. The body-cells 
have their enzymes, bactericidal, and bacteriolytic agents, 
opsonins and phagocytes. The phagocytes constitute the 


19 


290 CLINICAL MEDICINE FOR NURSES. 

mobile army of defense, and the fixed cells elaborate 
destructive weapons. Which of these bears the brunt of 
the defense depends upon the armament of the invader.” 

If the invasion is mainly bacterial in its nature, the 
leukocytes are called upon to play the principal part in 
winning the victory. If the invasion is mainly toxic, the 
tissue-cells have to bear the brunt of the defense. If the 
invasion is both bacterial and toxic, all the “arms of 
the service” play an equally important part in saving the 
body from destruction. 


GLOSSARY. 


Aeration. The state or process of being supplied with air or 
gas. 

Agglutinin. A specific principle occurring in the blood-serum 
of an animal affected with a disease of microbic origin, 
and capable of causing the clumping of the bacteria pecul¬ 
iar to that disease. 

Albuminuria. The presence of albumin in the urine. 

Alveolus. An air-cell of the lung. 

Ambulant. Referring to a patient that is up and about. Not 
confined to bed. 

Anemia. Deficiency of blood as a whole, or deficiency of the 
number of red corpuscles or of the hemoglobin. 

Anasarca. An accumulation of serum in the subcutaneous 
areolar tissues of the body. 

Anesthetic. Any drug that causes insensibility to pain. 

Anorexia. Loss of appetite. 

Antitoxin. A counterpoison or antidote manufactured by the 
body to counteract the toxins of bacteria. 

Anuria. Absence of secretion of urine. 

Aorta. The main arterial trunk of the body arising from the 
left ventricle of the heart. 

Aphasia. Partial or complete loss of the power of expressing 
ideas by means of speech or writing. 

Aphonia. Loss of the voice. 

Apoplexy. Hemorrhage from a blood-vessel in the brain. 

Arteriosclerosis. A chronic inflammation of the arterial walls 
resulting in more or less extensive fibrous tissue for¬ 
mation. 

Ascites. Fluid in the peritoneal cavity. 

Auricle. One of the two upper and smaller chambers of the 
heart. 

Bactericidal. Having the power of killing bacteria. 

( 291 ) 



GLOSSARY. 


Bacteriolytic. Possessing a disintegrating action upon living 
bacteria. 

Basophile. A leukocyte whose granules stain with basic dyes. 

Bronchitis. Inflammation or catarrh of the bronchial tubes. 

Buttock. The fleshy part of the body back of the hip-joint 
formed by the masses of the glutei muscles. 

Calorie. The amount of heat required to raise a kilogram of 
water, one degree Centigrade. 

Capillary. A minute blood-vessel connecting the smallest 
branches of the arteries with those of the veins. 

Carbohydrate. An organic substance containing 6 carbon 
atoms, or some multiple of 6 , and hydrogen and oxygen in 
the proportion in which they form water (H2O)—that is, 
twice as many hydrogen as oxygen atoms. (C 6 H 10 O 5 .) 

Carbon dioxid. A gas chemically known as CO 2 or carbonic 
acid gas. 

Cardiac. Relating or pertaining to the heart. 

Catharsis. Purgation. 

Chlorosis. A form of anemia most common in young women, 
characterized by a marked reduction of hemoglobin in the 
blood, with but slight diminution of red corpuscles. 

Chordae tendineae. The tendinous strings connecting the papil¬ 
lary muscles of the heart with the mitral and tricuspid 
valves. 

Chorea. A functional nervous disorder 1 usually occurring in 
youth, characterized by irregular and involuntary action 
of the muscles of the extremities, face, etc., with general 
muscular weakness. (Syn., St. Vitus’ Dance.) 

Cicatrization. Scar formation. 

Clinical. Relating to bedside treatment. 

Coma. Unconsciousness from which the patient cannot be 
aroused by external stimulus. 

Compensation. The extra work performed by a leaking heart 
in order to maintain the balance of the circulation. 

Crisis. The sudden termination of a fever. 

Cusp. A flap of a heart-valve. 

Cyanosis. A' bluish discoloration of the skin from deficient 
oxydation of the blood. 

Cyanotic. Referring to an individual exhibiting cyanosis. 


GLOSSARY. 293 

Cystitis. Inflammation of the urinary bladder. 

Delirium. A condition of mental excitement with confusion 
and usually hallucinations and delusions. 

Deoxygenated. Deprived of oxygen. 

Desquamation. A shedding of the superficial epithelium of 
the skin. “Peeling.” 

Detritus. Unrecognizable or formless waste matter. 

Diaphoresis. Sweating. 

Diaphragm. The muscular and tendinous plane separating 
the thorax from the abdomen. 

Diastole. The period of rest in the cardiac cycle. 

Dicrotic. The term applied to a pulse-beat in which with 
every wave the examining finger feels a double beat. 

Diffusible. Spreading to all parts of the body. 

Diplococcus. A coccus or round germ occurring in pairs. 

Diuretic. Any drug that increases the flow of urine. 

Dysphagia. Painful swallowing. 

Dyspnea. Shortness of breath. 

Edema. Presence of serum in the subcutaneous tissues. 

Embolus. A particle of fibrin or other material brought by 
the blood-current and forming an obstruction at its place 
of lodgment. 

Empyema. Pus in the pleural cavity. 

Endocarditis. Inflammation of the endocardium. 

Endocardium. The lining membrane of the heart. 

Engorgement. Congestion. 

Enzyme. A digestive ferment. 

Eosinophile. A leukocyte whose granules stain with acid 
dj r es. 

Epidemic. A term applied to a disease affecting a large num¬ 
ber or spreading over a wide area. 

Epiglottis. A cartilaginous structure situated behind the root 
of the tongue that prevents food and drink from passing 
into the larynx. 

Epithelium. A term applied to the group of cells that covers 
the skin and that lines all canals having communication 
with the external air, as the mouth, urethra, intestine, etc., 
and that are specialized for secretion in certain glands, as 
the liver, kidney, etc. 


294 


GLOSSARY 


Erosion. Eating away. 

Eruption. A rash. 

Erythrocyte. A red blood-corpuscle. 

Exophthalmic. Relating to exophthalmos. 

Exophthalmos. Protrusion of the eyeballs. 

Exudate. The material that has passed through the walls of 
blood-vessels into adjacent tissues. 

Febrile. Having fever. 

Feces. The movements of the bowels. 

Fibrin. A proteid found in blood after it has been shed, and 
constituting the main factor in the clotting of blood. 

Fibrosis. Formation of fibrous tissue. 

Flagellated. Bearing hair-like processes or flagellae. 

Focus. The location of an infection. 

Fomites. Any substance that absorbs and transmits a contagion. 

Gastric. Relating or pertaining to the stomach. 

General anasarca. Serum in the tissues, and in the peritoneal 
and pleural cavities. 

Germicide. Any substance having the power of killing germs. 

Glomerulus. One of the secreting elements in. the kidneys, 
lying in the cortex of that organ, and formed of a tuft of 
capillaries surrounded by a capsule (Bowman’s), and giv¬ 
ing off a uriniferous tubule. 

Goitre. A swelling of the thyroid gland not of inflammatory 
origin. 

Gout. A disease of metabolism characterized by attacks of 
pain in the small joints, and by a deposit therein of 
sodium urate. 

Hemophiliac. An individual in whose blood the power of 
clotting is reduced or absent—a “bleeder.” 

Hemoglobin. The coloring matter of the blood. Found in 
the red blood-corpuscles. 

Hemorrhagic. Pertaining to hemorrhage. Bloody. 

Hepatization. The name applied to the second and third 
stages in the consolidation of the lung in lobar pneu¬ 


monia. 


GLOSSARY. 


295 


Herpes. An acute inflammatory condition of the skin char¬ 
acterized by the development of a group of vesicles. 

Herpes zoster. An eruption occurring along the course of the 
intercostal nerves. (Syn., “Shingles.”) 

Hydrocephalus. A collection of fluid within the ventricles of 
the brain, or outside the brain, between it and the skull. 

Hydrotherapy. Treatment by means of water. 

Hydrothorax. Fluid in the pleural cavity. 

Hyperglycemia. An excess of sugar in the blood, i.e., when 
the amount of sugar is over 0.110 gram per 100 c.c. of 
blood. 

Hyperemia. Congestion. 

Hyperplasia. Excessive formation of tissue. An increase in 
the size of a tissue or organ owing to an increase in the 
number of cells. 

Hypertrophy. An increase in the size of a tissue or organ in¬ 
dependent of the general growth of the body. 

Hyperpyrexia. Excessively high fever—over 106° F. 

Hypertension. Blood-pressure that is above normal. 

Hypnotic. Any drug that produces sleep. 

Hypochondrium. The upper lateral region of the abdomen 
beneath the lower ribs. 

Hypodermoclysis. The subcutaneous injection of fluid. 

Hypoglycemia. A deficient amount of sugar in the blood, i.e., 
when the amount of sugar is less than 0.080 gram per 
100 c.c. of blood. 

Hypotension. Blood-pressure that is below normal. 

Incontinence. Lack of control over the contents of either 
bladder or rectum. 

Incubation. The period of a disease between the onset of the 
infection and the development of symptoms. 

Infection. (1) The communication of disease from one body 
to another. (2) The agent that produces disease. 

Infectious. Having the power of communicating disease. 

Infusion. The intravenous injection of salt solution. 

Ileum. The third portion of the small intestine. 

Immunity. The condition of the body in which it resists the 
development of disease. 

Inhibitory. Checking. Restraining. 


296 


GLOSSARY. 


Inoculation. The act of introducing the virus of a disease 
into the body. 

Insomnia. Inability to sleep. 

Intercostal. Relating to any structure situated between the 
ribs. 

Interstitial. Pertaining to interstitial or connective tissue. 

Intracranial. Situated within the skull. 

Invasion. The onset of a disease. 

Jejunum. The second portion of the small intestine. 

Koplik’s spots. Small bluish spots seen in cases of measles, 
and occurring on the mucous membrane of the cheeks and 
lips before the appearance of the rash. An absolutely 
diagnostic sign of measles. 

Laryngitis. Inflammation of the larynx. 

Leukocyte. A white blood-corpuscle. 

Leukocytosis. An increase in the number of leukocytes. 

Ligation. The tying of a blood-vessel. 

Lumen. The cavity surrounded by the walls of a tubular 
vessel. 

Lymphocyte. A variety of leukocyte having a very large 
nucleus and a relatively small cell-body. 

Lysis. The gradual disappearance of a fever. 

Macule. A spot upon the skin not elevated above the sur¬ 
rounding level. 

Malaise. A general feeling of illness, accompanied by rest¬ 
lessness and discomfort. 

Media. The middle coat of the wall of an artery. 

Megaloblast. A large nucleated red blood-corpuscle. 

Meninges. The dura mater, pia mater, and arachnoid mem¬ 
branes of the brain and spinal cord. 

Metabolism. The group of phenomena whereby organic be¬ 
ings transform foodstuffs into complex tissue-elements, 
and convert complex substances into simple ones in the 
production of heat and energy. 

Metastatic. Referring to metastasis, which is the transfer of 
a diseased process from one part of the body to another 
by means of the blood or lymph channels. 


GLOSSARY. 


297 


Meteorism. Gas in the intestines. 

Motile. Possessing the power of motion. 

Mucoid. Resembling mucus. 

Myocarditis. Inflammation of the heart-muscle. 

Myxedema. A disease of nutrition due to lack of secretion or 
absence of the thyroid gland. 

Necrosis. Death of tissue. 

Necrotic. Referring to necrosis. 

Nephritis. Inflammation of the kidneys. 

Neutrophile. A leukocyte whose granules stain with neutral 
dyes. 

Normoblast. A red blood-corpuscle of normal size having a 
nucleus. 

Nucleated. Possessing a nucleus. 

Nucleus. The essential part of a typical cell. 

Oliguria. A small amount of urine. 

Opsonin. A substance in blood-serum that prepares bacteria 
for digestion by leukocytes. 

Organic. Pertaining to the animal and vegetable world. 

Otitis. Inflammation of the ear. 

Oxydation. The act or process of combining with oxygen. 

Oxygen. A colorless, tasteless, odorless gas, composing one- 
fifth of atmospheric air, and in the absence of which 
human and animal life cannot be maintained. 

Palpitation. Consciousness of the heart-beat. 

Papule. A small circumscribed solid elevation of the skin. 

Paracentesis. Puncture of the wall of one of the cavities of 
the body, e.g., the ear, the pleura, the peritoneum. 

Parasite. An animal or vegetable living upon or within an¬ 
other individual, the host, e.g., malarial parasite, in red 
blood-corpuscles; tape-worm, in intestines. 

Parenchymatous. Referring to the parenchyma or specialized 
portion of an organ, as differentiated from the supporting 
and surrounding tissue. 

Pathogenic. Producing disease. 


298 


GLOSSARY. 


Pathological. Referring to pathology, which is that branch of 
medical science that treats of the modifications of func¬ 
tion and changes in structure caused by disease. 

Pericarditis. Inflammation of the pericardium. 

Pericardium. The membrane covering the heart and the root 
of the aorta and pulmonary artery. 

Peritoneum. The membrane lining the interior of. the ab¬ 
dominal cavity and surrounding the contained viscera or 
organs. 

Peritonitis. Inflammation of the peritoneum. 

Phagocytosis. The process of ingestion and digestion of 
micro-organisms by the leukocytes. 

Phlebitis. Inflammation of a vein. 

Physiology. The science of the normal workings of the 
human body. 

Pitting. The formation of a pit or hollow by pressure upon 
edematous subcutaneous tissue. 

Pleura. The membrane surrounding the lung. 

Pleurisy. Inflammation of the pleura. 

Pneumococcus. The causative factor in lobar pneumonia. 

Pneumonia. Inflammation of the lung. 

Pneumothorax. Air in the pleural cavity. 

Poikilocytosis. Irregularity in outline of red blood-corpuscles. 

Polymorphonuclear. A leukocyte having nuclei of varied 
shapes and sizes. 

Polyuria. An excessive amount of urine. 

Precipitin. A substance present in blood-serum capable of 
producing a precipitate in a clear solution of the particular 
albumin or culture filtrate against which the individual 
whose blood is used, has been immunized. 

Prophylactic. Preventive. 

Proteid. Any of the important and essential nitrogenous con¬ 
stituents of animal and vegetable tissues. 

Ptosis. A drooping or sagging. May refer to drooping of the 
eyelid or to a general sagging down of the abdominal 
viscera. 

Purulent. Containing pus. 

Pus. A liquid substance consisting of cells and an albuminous 
fluid formed in certain kinds of inflammation. 


GLOSSARY. 299 

Pyemia. A disease due to the presence in the blood of pus¬ 
forming germs. 

Pyelonephritis. Inflammation of the kidney and its pelvis. 

Receptor. One of the so-called “side arms” of a cell, which 
according to Ehrlich’s “side chain” theory of immunity is 
for protection of the cell by uniting with an attacking 
molecule of toxin. 

Regurgitation. The back-flow of blood through a heart valve 
that is defective. 

Remission. A fall in fever in which, however, the temperature 
still remains above normal. 

Resection. The process of cutting out and removing. 

Resolution. The fourth stage in the evolution of the process 
undergone by the inflamed lung in lobar pneumonia. 

Sedative. A drug whose actfon is to quiet the patient. 

Semilunar. The valves guarding the openings of the aorta 
and pulmonary artery. 

Sepsis, Blood-poisoning. 

Septicemia. Blood-poisoning. 

Serous. Relating to serum. 

Serum. The clear yellow fluid that separates itself from the 
clot after the shedding of blood. 

Sordes. The crusts that accumulate on the teeth and lips in 
continued fevers. 

Splanchnic. Pertaining to or supplying the viscera. 

Sputum. The secretion of the lungs and bronchi. 

Stenosis. Constriction of a heart valve, as a result of which it 
cannot open as fully as it should. 

Stippling. A term used to describe a peculiar spotted appear¬ 
ance of red blood-corpuscles in severe anemias. 

Striated. Possessing striae or stripe-like lines. 

Stupe. A cloth used for applying heat or counterirritation. 

Stupor. A state of partial unconsciousness from which the 
victim can be roused. 

Systole. The period of contraction or “work-period” of the 
heart. 


300 


GLOSSARY. 


Tachycardia. Excessively rapid heart-action. 

Thrombosis. The formation of a thrombus. 

Thrombus. A clot of blood formed within the heart or blood¬ 
vessels. 

Toxemia. Blood-poisoning. A condition in which the blood 
contains poisonous products, either those produced by the 
body-cells, or those due to the growth of micro-organisms. 

Toxin. A poison. 

Tracheotomy. The operation of opening the trachea or wind¬ 
pipe and inserting a tube through which the patient can 
breathe. 

Tremor. A trembling of the voluntary muscles. 

Tubercle. The specific lesion produced by the tubercle 
bacillus. 


Vagus. The 10th pair of cranial nerves. 

Vascular. Pertaining or relating to the circulatory system. 

Vasodilator. A drug causing dilatation of the arteries and 
consequent lowering of blood-pressure. 

Venesection. The operation of opening a vein in order to 
allow the escape of a certain amount of blood. “Bleeding." 

Ventricle. (1) One of the two lower larger chambers of the 
heart. (2) One of several spaces in the brain. 

Virulent. Having the nature of a poison. 

Vomitus. The material that is vomited. 


INDEX 


Agglutinin, 288 
Albuminoids, 5 
Albuminuria, 75 
Anemia, pernicious, 278 
in rheumatic fever, 22 
symptoms, 278 
Aneurysm, 62 
course, 64 
symptoms, 63 
treatment, 65 
Anorexia, 1 
Antitoxin, 237 
Aorta, 14, 17 
aneurysm of, 62 
Apoplexy, 115 
Arteriosclerosis, 101 
pathology, 102 
treatment, 106 
Artery, 13, 14 
pulmonary, 15 

Artificial pneumothorax, 219 
Auricle, 15, 17 
Auricular fibrillation, 49 

Blood, the, 272 
clotting of, 272 
in leukemia, 280 
in pernicious anemia, 279 
plasma, 272 
pressure, 66 
abnormal, 70 
determination of, 66 
diastolic, 69 


Blood-pressure, normal, 69 
systolic, 68 

Bright’s disease. See Neph¬ 
ritis. 

Calcium, 4 
Calorie, 17 
Capillary, 13, 14 
pulmonary, 15 
pulse, 48 

Capsule of Glisson, 16 
Carbohydrate, 4, 5, 6 
tolerance in diabetes, 263 
Carbon, 5 
dioxide, 17 
Cardiac cycle, 18 
Catharsis, 94 
Cell, endothelial, 17 
red blood, 17, 274 
Cerebrospinal meningitis, 246 
Kernig’s sign in, 247 
lumbar puncture in, 248 
pathology, 246 
symptoms, 247 
treatment, 249 
Chordae tendinae, 20 
Chorea, 22, 24 
Circulation, the, 13 
greater or systemic, 15 
lesser or pulmonary, 16 
portal or splanchnic, 16 
Collapse, treatment of, in lo¬ 
bar pneumonia, 140 

(301) 




302 


INDEX. 


Compensation, 43, 44, 45 
Cusp, 20 

Diabetes mellitus, 260 
complications, 261 
insulin in, 268 
prognosis, 261 
symptoms, 260 
treatment, 262 
Diaphoresis, 94 
Diastole, 18 

Diet, in acute nephritis, 95 
in chronic nephritis with 
edema, 99 
in diabetes, 262 
in pneumonia, 137 
in rheumatic fever, 26 
in tuberculosis, 210 
in typhoid, 178 
Digitalis, effect on heart, 53 
Diphtheria, 233 
complications, 234 
prognosis, 236 
symptoms, 233 
laryngeal, 234 
pharyngeal, 233 
treatment, 236 
with antitoxin, 237 

Endocarditis, 36 
chronic, 42 

compensation in, 43, 44, 45 
digitalis in, 50, 51 
nature of process in, 46 
prognosis, in, 50 
symptoms, 46 
treatment, 51 
etiology, 36 
malignant, 40 
treatment, 40 


Endocarditis, pathology, 37 
prognosis, 39 
simple, 36 
symptoms, 37 
treatment, 41 
Endocardium, 20 
Erythrocyte, 274 
Exophthalmic goitre, 282 
symptoms, 283 
treatment, 284 
Extractives, 5 

Fat, 4, 5, 6 
Fever, 1, 2 

Food, 4. See also Diet. 

Gelatinoids, 5 
Glisson’s capsule, 16 
Graves’ disease. See Exoph¬ 
thalmic Goitre. 
Glycosuria, 76, 260 

Heart, 17 
Hemoglobin, 276 
Hemoptysis, 201 
Hemorrhage, cerebral, 115 
symptoms, 115 
treatment, 117 
pulmonary, 201 
treatment, 214 
typhoidal, 169 
treatment, 185 
Hydrogen, 5 
Hydrotherapy, 182 
Hyperpyrexia, 3, 23 
Hypertension, 70 
Hypotension, 70 

Immunity, 286 
active, 288 



INDEX. 


303 


Immunity, passive, 289 
phagocytosis in, 287 
side chain theory of, 288 
Indicanuria, 76 
Influenza, 147 
complications, 150 
prognosis, 151 
symptoms, 148 
treatment, 152 
insulin, 268 

Intestinal tuberculosis, 203 
Intubation, 240 

Kernig’s sign, 247 

Laryngitis, diphtheritic, 234 
tuberculous, 202 
Leukemia, 280 
Leukocyte, 274 
Leukocytosis, 275 
Liver, 16 

Locomotor ataxia, 257 
symptoms, 257 
treatment, 259 
Lumbar puncture, 248 

Magnesium, 4 
Measles, 227 
complications, 229 
prophylaxis, 231 
symptoms, 228 
treatment, 231 

Meningitis, cerebrospinal, 246 
tuberculous, 204 
Myocarditis, 21, 23, 59 
acute, 59 
chronic, 60 

Nephritis, 87 
acute, 87 


Nephritis, acute, catharsis in, 
94 

complicating scarlet fever, 
223 

diaphoresis in, 94 
diet in, 95 
diuretics in, 93 
etiology, 88 
pathology, 88 
symptoms, 89 
treatment, 92 
urine in, 90 

chronic without edema, 101 
pathology, 102 
symptoms, 104 
cardiac, 105 
toxic, 104 
urinary, 104 
treatment, 106 
chronic with edema, 97 
diet in, 99 

fluid restrictions in, 100 
general management, 98 
salt restriction in, 100 
symptoms, 97 
treatment, 98 
Nerve, vagus, 18 
Nitrogen, 4, 5 

Oliguria, 70 
Opsonin, 288 

Otitis media, complicating 
measles, 229 
scarlet fever, 224 
Oxygen, 13 

Pericarditis, 30 
dry, 32 

symptoms, 32 
etiology, 30 



304 


INDEX. 


Pericarditis, pathology, 31 
treatment, 34 
dry, 34 

with effusion, 35 
with effusion, 33 
Pericardium, 30 
Perforation in typhoid, 170 
Phagocytosis, 287 
Phenolsulphonephthalein test, 
110 

Physiology of respiration, 16 
Pleura, 119 
Pleural cavity, 120 
Pleurisy, 119 
dry, 120 

symptoms, 121 
treatment, 121 
with effusion, 123 
symptoms, 123 
treatment, 124 
Pneumonia, broncho-, 142 
complicating measles, 229 
in the aged, 144 
in children, 142 
symptoms, 142 
treatment, 144 
Pneumonia, lobar, 126 
bowels in, 134, 137 
blood in, 134 
circulation in, 138 
collapse in, 139 
complicating rheumatic fe¬ 
ver, 24 

complications, 135 
cough in, 133, 137 
crisis in, 130 
diet in, 137 
etiology, 126 
fever in, 130, 137 
fresh air in, 136 


Pneumonia, lobar, heart in, 132 
herpes in, 134 
pain in, 129 
pathology, 127 
pulse in, 131 
respiration in, 133 
specific treatment in, 139 
sputum in, 133 
symptoms, 129 
treatment, 135 
typical attack, 129 
urine in, 134 

Poliomyelitis, anterior, 241 
etiology, 241 
pathology, 242 
prophylaxis, 244 
symptoms, 242 
treatment, 245 
Polyuria, 75 
Potassium, 4 
Protein, 4, 6 
Pyuria, 76 

Regurgitation, 19 
aortic, 43 
mitral, 43 

Renal function tests, 109 
phenolsulphonephthalein test, 
110 

specific gravity test, 111 
technique of, 112 
Rheumatic fever, 21 
cardiac affections in, 23 
complications, 23 
hyperpyrexia in, 23 
joints in, 22 
symptoms, 22 
treatment, 25 
bed in, 25 
diet in, 26 



INDEX. 


305 


Rheumatic fever, drugs in, 26 
symptomatic, 28 

Salicylic acid, 26 
Salt, 4 

restriction in nephritis, 100 
Scarlet fever, 221 
acute nephritis in, 223 
complications, 223 
otitis media in, 224 
prophylaxis, 224 
rash in, 222 
symptoms, 221 
treatment, 226 
Sodium, 4 

Specific gravity test, 111 
of urine, 72 

Sphygmomanometer, 66 

Starch, 5 

Stenosis, aortic, 43 
mitral, 43 
Streptococcus, 21 
Syphilis, 251 
Systole, 18 

Test, renal function, 109 

phenolsulphonephthalein, 

110 

specific gravity, 111 
albumin in urine, 75 
reaction of urine, 75 
specific gravity of urine, 72 
sugar in urine, 76 
Thrombosis, cerebral, 118 
in typhoid, 171 
Tonsillitis, 22 
Tracheotomy, 240 
Tubercle, the, 192 
Tuberculosis, 188 
acute, 193 


Tuberculosis, acute, general 
miliary, 193 
miliary of lungs, 194 
artificial pneumothorax in, 
219 

chronic, 196 
complications of, 201 
enteritis, 203 
hemoptysis, 201 
laryngitis, 202 
meningitis, 204 
environment in, 192 
etiology, 190 
history, 188 
pathology, 192 
prophylaxis, 205 
individual, 206 
pneumonia, acute tuber¬ 
culous, 195 
pulmonary, 194 
varieties of, 176 
symptoms, 194, 197 
treatment, 208 
food in, 210 

general management, 209 
bowels, 211 
cough, 212 
insomnia, 213 
night-sweats, 213 
temperature, 212 
vomiting, 213 
of hemorrhage, 214 
of laryngitis, 216 
tuberculin in, 218 
Typhoid fever, 155 
blood in, 167 
complications in, 169 
diet in, 178 
diarrhea in, 172 
etiology, 159 


20 





306 


INDEX. 


Typhoid fever, hemorrhage in, 
169 

high calorie diet in, 180 
history, 155 
hydrotherapy in, 182 
lobar pneumonia in, 171 
pathology, 161 
perforation, 170 
preventive inoculation in, 

177 

prognosis, 173 
prophylaxis, 174 
rose spots in, 164 
stools in, 168 
symptoms, 164 
1st week, 164 
2d week, 166 
3d week, 166 
4th week, 167 
treatment, 178 
of complications, 185 
urine in, 167 
water in, 181 
Widal reaction in, 167 


Uremia, 82 
acute, 82 
chronic, 83 
Urine, 72 
abnormal, 74 
collection of, 76 
examination of, 78 
normal, 73 

Valve, 13 
aortic, 19 
cardiac, 18 
mitral, 19 
pulmonary, 19 
tricuspid, 19 
Vein, 13, 14 
hepatic, 16 
portal, 16 
pulmonary, 15 
Vena cava, 14, 17 
Ventricle, 14, 15, 17 

Water, 4 

Widal reaction, 167 


























































